„Hygienehypothese“ – Versionsunterschied

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AZ: Die Seite wurde neu angelegt: In der Medizin besagt die '''Hygienehypothese''', dass die frühkindliche Exposition gegenüber bestimmten Mikroorganismen (wie der Darmflora und Helminthenparasiten) vor allergischen Erkrankungen schützt, indem sie zur Entwicklung des Immunsystems beitragen.<ref name=":1">{{Literatur |Autor=Megan Scudellari |Titel=News Feature: Cleaning up the hygiene hypothesis |S…
Markierung: 2017-Quelltext-Bearbeitung
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In der Medizin besagt die '''Hygienehypothese''', dass die frühkindliche Exposition gegenüber bestimmten Mikroorganismen (wie der [[Darmflora]] und Helminthenparasiten) vor [[Allergie|allergischen]] Erkrankungen schützt, indem sie zur Entwicklung des [[Immunsystem|Immunsystems]] beitragen.<ref name=":1">{{Literatur |Autor=Megan Scudellari |Titel=News Feature: Cleaning up the hygiene hypothesis |Sammelwerk=Proceedings of the National Academy of Sciences of the United States of America |Band=114 |Nummer=7 |Datum=2017-02-14 |ISSN=1091-6490 |DOI=10.1073/pnas.1700688114 |PMC=5320962 |PMID=28196925 |Seiten=1433–1436 |Online=https://pubmed.ncbi.nlm.nih.gov/28196925/ |Abruf=2022-03-31}}</ref><ref name=":2">{{Literatur |Autor=Leah T. Stiemsma, Lisa A. Reynolds, Stuart E. Turvey, B. Brett Finlay |Titel=The hygiene hypothesis: current perspectives and future therapies |Sammelwerk=ImmunoTargets and Therapy |Band=4 |Datum=2015 |ISSN=2253-1556 |DOI=10.2147/ITT.S61528 |PMC=4918254 |PMID=27471720 |Seiten=143–157 |Online=https://pubmed.ncbi.nlm.nih.gov/27471720/ |Abruf=2022-03-31}}</ref> Insbesondere wird angenommen, dass eine mangelnde Exposition zu Defekten bei der Etablierung der [[Immuntoleranz]] führt. Der Zeitraum für die Exposition beginnt in utero und endet im Schulalter.<ref>{{Literatur |Autor=Caroline Roduit, Remo Frei, Erika von Mutius, Roger Lauener |Titel=The Hygiene Hypothesis |Sammelwerk=Environmental Influences on the Immune System |Verlag=Springer |Ort=Vienna |Datum=2016 |ISBN=978-3-7091-1890-0 |DOI=10.1007/978-3-7091-1890-0_4 |Seiten=77–96}}</ref>
{{Short description|Medical hypothesis on development of immunity}}
{{Use dmy dates|date=October 2013}}


Während sich frühe Versionen der Hypothese auf die Exposition gegenüber Mikroben im Allgemeinen bezogen, gelten aktualisierte Versionen für eine bestimmte Gruppe mikrobieller Arten, die sich [[Koevolution|gemeinsam]] mit dem Menschen [[Koevolution|entwickelt]] haben.<ref name=":1" /><ref name=":2" /><ref name=":4">{{Literatur |Autor=Gabriel M. Alexandre-Silva, Pablo A. Brito-Souza, Ana C. S. Oliveira, Felipe A. Cerni, Umberto Zottich |Titel=The hygiene hypothesis at a glance: Early exposures, immune mechanism and novel therapies |Sammelwerk=Acta Tropica |Band=188 |Datum=2018-12 |ISSN=1873-6254 |DOI=10.1016/j.actatropica.2018.08.032 |PMID=30165069 |Seiten=16–26 |Online=https://pubmed.ncbi.nlm.nih.gov/30165069/ |Abruf=2022-03-31}}</ref> Die Aktualisierungen wurden mit verschiedenen Namen versehen, darunter die Hypothese des Mikrobiommangels, die Mikroflora-Hypothese und die Hypothese der „alten Freunde“.<ref name=":4" /><ref>{{Internetquelle |url=https://evmedreview.com/reconstituting-the-depleted-biome-to-prevent-immune-disorders/ |titel=Reconstituting the depleted biome to prevent immune disorders |datum=2010-10-13 |sprache=en-US |abruf=2022-03-31}}</ref> Es gibt eine beträchtliche Menge an Beweisen, die die Idee stützen, dass die mangelnde Exposition gegenüber diesen Mikroben mit Allergien oder anderen Erkrankungen zusammenhängt<ref name=":2" /><ref>{{Literatur |Autor=D. Daley |Titel=The evolution of the hygiene hypothesis: the role of early-life exposures to viruses and microbes and their relationship to asthma and allergic diseases |Sammelwerk=Current opinion in allergy and clinical immunology |Datum=2014 |DOI=10.1097/ACI.0000000000000101 |Online=https://www.semanticscholar.org/paper/The-evolution-of-the-hygiene-hypothesis%3A-the-role-Daley/0921ea76399f2f8e6775bc1c76d1b7cd418ca696 |Abruf=2022-03-31}}</ref><ref>{{Literatur |Autor=Mathilde Versini, Pierre-Yves Jeandel, Tomer Bashi, Giorgia Bizzaro, Miri Blank |Titel=Unraveling the Hygiene Hypothesis of helminthes and autoimmunity: origins, pathophysiology, and clinical applications |Sammelwerk=BMC medicine |Band=13 |Datum=2015-04-13 |ISSN=1741-7015 |DOI=10.1186/s12916-015-0306-7 |PMC=4396177 |PMID=25879741 |Seiten=81 |Online=https://pubmed.ncbi.nlm.nih.gov/25879741/ |Abruf=2022-03-31}}</ref>, obwohl es immer noch wissenschaftliche Meinungsverschiedenheiten gibt.<ref name=":4" /><ref name=":8">{{Literatur |Autor=Bengt Björkstén |Titel=The hygiene hypothesis: do we still believe in it? |Sammelwerk=Nestle Nutrition Workshop Series. Paediatric Programme |Band=64 |Datum=2009 |ISSN=1661-6677 |DOI=10.1159/000235780 |PMID=19710512 |Seiten=11–18; discussion 18–22, 251-257 |Online=https://pubmed.ncbi.nlm.nih.gov/19710512/ |Abruf=2022-03-31}}</ref><ref name=":9">{{Literatur |Autor=Erik van Tilburg Bernardes, Marie-Claire Arrieta |Titel=Hygiene Hypothesis in Asthma Development: Is Hygiene to Blame? |Sammelwerk=Archives of Medical Research |Band=48 |Nummer=8 |Datum=2017-11 |ISSN=1873-5487 |DOI=10.1016/j.arcmed.2017.11.009 |PMID=29224909 |Seiten=717–726 |Online=https://pubmed.ncbi.nlm.nih.gov/29224909/ |Abruf=2022-03-31}}</ref>
In medicine, the '''hygiene hypothesis''' states that early childhood exposure to particular microorganisms (such as the [[gut flora]] and [[helminth]] parasites) protects against [[allergy|allergic]] diseases by contributing to the development of the [[immune system]].<ref name=":0">{{Cite journal |doi=10.1073/pnas.1700688114 |pmid=28196925 |pmc=5320962 |bibcode=2017PNAS..114.1433S |title=News Feature: Cleaning up the hygiene hypothesis |journal=Proceedings of the National Academy of Sciences |volume=114 |issue=7 |pages=1433–1436 |last1=Scudellari |first1=Megan |year=2017 |doi-access=free }}</ref><ref name="StiemsmaReynolds2015"/> In particular, a lack of exposure is thought to lead to defects in the establishment of [[immune tolerance]].<ref name=":0"/> The time period for exposure begins ''in utero'' and ends at school age.<ref name="RoduitFrei2016">{{cite book |doi=10.1007/978-3-7091-1890-0_4 |chapter=The Hygiene Hypothesis |title=Environmental Influences on the Immune System |year=2016 |last1=Roduit |first1=Caroline |last2=Frei |first2=Remo |last3=von Mutius |first3=Erika |last4=Lauener |first4=Roger |pages=77–96 |isbn=978-3-7091-1888-7 }}</ref>


Der Begriff ''Hygienehypothese'' wurde als falsche Bezeichnung beschrieben, weil die Leute ihn fälschlicherweise so interpretieren, dass er sich auf persönliche Sauberkeit bezieht.<ref name=":1" /><ref name=":8" /><ref>{{Literatur |Autor=M. Wendel-Haga, E. G. Celius |Titel=Is the hygiene hypothesis relevant for the risk of multiple sclerosis? |Sammelwerk=Acta Neurologica Scandinavica |Band=136 Suppl 201 |Datum=2017-11 |ISSN=1600-0404 |DOI=10.1111/ane.12844 |PMID=29068485 |Seiten=26–30 |Online=https://pubmed.ncbi.nlm.nih.gov/29068485/ |Abruf=2022-03-31}}</ref><ref>{{Literatur |Autor=William Parker |Titel=The “hygiene hypothesis” for allergic disease is a misnomer |Sammelwerk=BMJ : British Medical Journal |Datum=2014 |DOI=10.1136/bmj.g5267 |Online=https://www.semanticscholar.org/paper/The-%E2%80%9Chygiene-hypothesis%E2%80%9D-for-allergic-disease-is-a-Parker/1c2ef5ae32e79d33832f29e7e095829efcfa07a9 |Abruf=2022-03-31}}</ref> Es wird erwartet, dass die Reduzierung der persönlichen Hygiene, wie z. B. das Nichtwaschen der Hände vor dem Essen, einfach das Infektionsrisiko erhöht, ohne Auswirkungen auf Allergien oder Immunstörungen zu haben.<ref name=":1" /><ref name=":8" /><ref name=":9" /> Hygiene ist unerlässlich, um gefährdete Bevölkerungsgruppen wie ältere Menschen vor Infektionen zu schützen, die Ausbreitung von Antibiotikaresistenzen zu verhindern und [[Emerging Infectious Disease|neu auftretende Infektionskrankheiten]] wie [[Ebolavirus|Ebola]] oder [[COVID-19]] zu bekämpfen.<ref>{{Literatur |Autor=Sally F. Bloomfield, Graham Aw Rook, Elizabeth A. Scott, Fergus Shanahan, Rosalind Stanwell-Smith |Titel=Time to abandon the hygiene hypothesis: new perspectives on allergic disease, the human microbiome, infectious disease prevention and the role of targeted hygiene |Sammelwerk=Perspectives in Public Health |Band=136 |Nummer=4 |Datum=2016-07 |ISSN=1757-9147 |DOI=10.1177/1757913916650225 |PMC=4966430 |PMID=27354505 |Seiten=213–224 |Online=https://pubmed.ncbi.nlm.nih.gov/27354505/ |Abruf=2022-03-31}}</ref> Die Hygienehypothese deutet nicht darauf hin, dass mehr Infektionen während der Kindheit ein Gesamtnutzen wären.<ref name=":1" /><ref name=":8" />
While early versions of the hypothesis referred to exposure to microbes in general, updated versions apply to a specific set of microbial species that have [[Coevolution|co-evolved]] with humans.<ref name=":0"/><ref name="Silva2018"/><ref name="StiemsmaReynolds2015">{{cite journal |last1=Stiemsma |first1=Leah |last2=Reynolds |first2=Lisa |last3=Turvey |first3=Stuart |last4=Finlay |first4=Brett |title=The hygiene hypothesis: Current perspectives and future therapies |journal=ImmunoTargets and Therapy |date=July 2015 |volume=4 |pages=143–157 |doi=10.2147/ITT.S61528 |pmid=27471720 |pmc=4918254 }}</ref> The updates have been given various names, including the [[Human microbiota|microbiome]] depletion hypothesis, the microflora hypothesis, and the "old friends" hypothesis.<ref name="Silva2018">{{cite journal |last1=Alexandre-Silva |first1=Gabriel M. |last2=Brito-Souza |first2=Pablo A. |last3=Oliveira |first3=Ana C.S. |last4=Cerni |first4=Felipe A. |last5=Zottich |first5=Umberto |last6=Pucca |first6=Manuela B. |title=The hygiene hypothesis at a glance: Early exposures, immune mechanism and novel therapies |journal=Acta Tropica |date=December 2018 |volume=188 |pages=16–26 |doi=10.1016/j.actatropica.2018.08.032 |pmid=30165069 }}</ref><ref name=parker>{{cite journal |title=Reconstituting the depleted biome to prevent immune disorders |journal=The Evolution and Medicine Review |date=13 October 2010 |url=https://evmedreview.com/reconstituting-the-depleted-biome-to-prevent-immune-disorders/ }}</ref> There is a significant amount of evidence supporting the idea that lack of exposure to these microbes is linked to allergies or other conditions,<ref name="StiemsmaReynolds2015"/><ref name="Daley2014"/><ref name="VersiniJeandel2015"/> although scientific disagreement still exists.<ref name="Silva2018"/><ref name="Bjorksten2009"/><ref name="Bernardes2017"/>


== Siehe auch ==
The term "hygiene hypothesis" has been described as a misnomer because people incorrectly interpret it as referring to personal cleanliness.<ref name=":0"/><ref name="Bjorksten2009">{{cite book |doi=10.1159/000235780 |chapter=The Hygiene Hypothesis: Do we still believe in it? |title=Microbial Host-Interaction: Tolerance versus allergy |series=Nestlé Nutrition Institute Workshop Series: Pediatric Program |year=2009 |last1=Björkstén |first1=Bengt |volume=64 |pages=11–22 |pmid=19710512 |isbn=978-3-8055-9167-6}}</ref><ref name="Haga2017">{{cite journal |last1=Wendel-Haga |first1=M. |last2=Celius |first2=E.G. |title=Is the hygiene hypothesis relevant for the risk of multiple sclerosis? |journal=Acta Neurologica Scandinavica |date=November 2017 |volume=136 |pages=26–30 |doi=10.1111/ane.12844 |pmid=29068485 |doi-access=free }}</ref><ref name="Parker2014">{{cite journal |last1=Parker |first1=W. |title=The 'hygiene hypothesis' for allergic disease is a misnomer |journal=BMJ |date=26 August 2014 |volume=349 |issue=aug26 2 |pages=g5267 |doi=10.1136/bmj.g5267 |pmid=25161287|s2cid=33624127 }}</ref> Reducing personal hygiene, such as not washing hands before eating, is expected to simply increase the risk of infection without having any impact on allergies or immune disorders.<ref name=":0"/><ref name="Silva2018"/><ref name="Bernardes2017">{{cite journal |last1=van Tilburg Bernardes |first1=Erik |last2=Arrieta |first2=Marie-Claire |title=Hygiene Hypothesis in Asthma Development: Is Hygiene to Blame? |journal=Archives of Medical Research |date=November 2017 |volume=48 |issue=8 |pages=717–726 |doi=10.1016/j.arcmed.2017.11.009 |pmid=29224909}}</ref> Hygiene is essential for protecting vulnerable populations such as the elderly from infections, preventing the spread of [[antibiotic resistance]], and for combating [[emerging infectious diseases]] such as [[Ebola]] or [[COVID-19]].<ref name="BloomfieldRook2016"/> The hygiene hypothesis does not suggest that having more infections during childhood would be an overall benefit.<ref name=":0"/><ref name="Bjorksten2009"/>
* [[Zivilisationskrankheit]]
* [[Keimtheorie]]
* [[Hakenwürmer]]


== Overview ==
== Literatur ==
* {{Literatur |Autor=Rob R. Dunn |Titel=Never home alone : from microbes to millipedes, camel crickets, and honeybees, the natural history of where we live |Auflage=First edition |Ort=New York, NY |Datum=2018 |ISBN=978-1-5416-4576-9}}
* {{Literatur |Autor=B. Brett Finlay |Titel=Let them eat dirt : saving your child from an oversanitized world |ISBN=9781616207380}}
* {{Literatur |Autor=Caroline Hadley |Titel=Should auld acquaintance be forgot.. |Sammelwerk=EMBO reports |Band=5 |Nummer=12 |Datum=2004-12 |ISSN=1469-221X |DOI=10.1038/sj.embor.7400308 |PMC=1299202 |PMID=15577925 |Seiten=1122–1124 |Online=https://pubmed.ncbi.nlm.nih.gov/15577925/ |Abruf=2022-03-31}}
* {{Literatur |Autor=G. a. W. Rook, L. R. Brunet |Titel=Microbes, immunoregulation, and the gut |Sammelwerk=Gut |Band=54 |Nummer=3 |Datum=2005-03 |ISSN=0017-5749 |DOI=10.1136/gut.2004.053785 |PMC=1774411 |PMID=15710972 |Seiten=317–320 |Online=https://pubmed.ncbi.nlm.nih.gov/15710972/ |Abruf=2022-03-31}}
* {{Literatur |Autor=G. Rook, V. Adams, J. Hunt, R. Palmer, R. Martinelli |Titel=Mycobacteria and other environmental organisms as immunomodulators for immunoregulatory disorders |Sammelwerk=Springer Seminars in Immunopathology |Datum=2003 |DOI=10.1007/s00281-003-0148-9 |Online=https://www.semanticscholar.org/paper/Mycobacteria-and-other-environmental-organisms-as-Rook-Adams/9dcf7be7e3490caa585b8c6844163d8874d6af99 |Abruf=2022-03-31}}


== Einzelnachweise ==
The idea of a link between parasite infection and immune disorders was first suggested in 1968.<ref name="MaizelsMcSorley2014">{{cite journal |last1=Maizels |first1=R. M. |last2=McSorley |first2=H. J. |last3=Smyth |first3=D. J. |title=Helminths in the hygiene hypothesis: sooner or later? |journal=Clinical & Experimental Immunology |date=July 2014 |volume=177 |issue=1 |pages=38–46 |doi=10.1111/cei.12353 |pmid=24749722 |pmc=4089153 }}</ref> The original formulation of the hygiene hypothesis dates from 1989, when David Strachan proposed that lower incidence of [[infection]] in early childhood could be an explanation for the rise in allergic diseases such as [[asthma]] and [[hay fever]] during the 20th century.<ref name=strachan2000>{{cite journal |last1=Strachan |first1=D. |title=Family size, infection and atopy: the first decade of the 'hygiene hypothesis' |journal=Thorax |date=1 August 2000 |volume=55 |issue=90001 |pages=2S–10 |doi=10.1136/thorax.55.suppl_1.s2 |pmid=10943631 |pmc=1765943 }}</ref>
<references responsive>
</references>


[[Kategorie:Allergologie]] [[Kategorie:Epidemiologie]]
The hygiene hypothesis has also been expanded beyond allergies, and is also studied in the context of a broader range of conditions affected by the immune system, particularly [[inflammatory disease]]s.<ref name="ShuYuen2018">{{cite journal |last1=Shu |first1=Shang-An |last2=Yuen |first2=Agatha W. T. |last3=Woo |first3=Elena |last4=Chu |first4=Ka-Hou |last5=Kwan |first5=Hoi-Shan |last6=Yang |first6=Guo-Xiang |last7=Yang |first7=Yao |last8=Leung |first8=Patrick S. C. |title=Microbiota and Food Allergy |journal=Clinical Reviews in Allergy & Immunology |date=18 December 2018 |volume=57 |issue=1 |pages=83–97 |doi=10.1007/s12016-018-8723-y |pmid=30564985 |s2cid=56476417 }}</ref> These include [[type 1 diabetes]],<ref name=stene2001>{{cite journal |last1=Stene |first1=Lars C |last2=Nafstad |first2=Per |title=Relation between occurrence of type 1 diabetes and asthma |journal=The Lancet |date=February 2001 |volume=357 |issue=9256 |pages=607–608 |doi=10.1016/S0140-6736(00)04067-8 |pmid=11558491 |s2cid=7457497 }}</ref> multiple sclerosis,<ref name=raison2010>{{cite journal |last1=Raison |first1=Charles L. |last2=Lowry |first2=Christopher A. |last3=Rook |first3=Graham A. W. |title=Inflammation, Sanitation, and Consternation |journal=Archives of General Psychiatry |date=December 2010 |volume=67 |issue=12 |pages=1211–1224 |doi=10.1001/archgenpsychiatry.2010.161 |pmid=21135322 |pmc=3724429 }}</ref><ref name="Haga2017"/> and also some types of depression<ref name=raison2010 /><ref name=rook2013>{{cite journal |last1=Rook |first1=Graham A. W. |last2=Lowry |first2=Christopher A. |last3=Raison |first3=Charles L. |title=Microbial 'Old Friends', immunoregulation and stress resilience |journal=Evolution, Medicine, and Public Health |date=2013 |volume=2013 |issue=1 |pages=46–64 |doi=10.1093/emph/eot004 |pmid=24481186 |pmc=3868387 }}</ref> and cancer.<ref name=rook2011>{{cite journal |last1=Rook |first1=Graham A. W. |last2=Dalgleish |first2=Angus |title=Infection, immunoregulation, and cancer |journal=Immunological Reviews |date=March 2011 |volume=240 |issue=1 |pages=141–159 |doi=10.1111/j.1600-065X.2010.00987.x |pmid=21349092 |s2cid=39495585 }}</ref>{{specify|date=March 2015}} For example, the global distribution of multiple sclerosis is negatively correlated with that of the helminth ''[[Trichuris trichiura]]'' and its incidence is negatively correlated with ''[[Helicobacter pylori]]'' infection.<ref name="Haga2017"/> Strachan's original hypothesis could not explain how various allergic conditions spiked or increased in prevalence at different times, such as why respiratory allergies began to increase much earlier than food allergies, which did not become more common until near the end of the 20th century.<ref name="BloomfieldRook2016"/>

In 2003 Graham Rook proposed the "old friends hypothesis" which has been described as a more rational explanation for the link between microbial exposure and inflammatory disorders.<ref name=rook2003>{{cite journal |last1=Rook |first1=Graham A.W. |last2=Martinelli |first2=Roberta |last3=Brunet |first3=Laura Rosa |title=Innate immune responses to mycobacteria and the downregulation of atopic responses |journal=Current Opinion in Allergy and Clinical Immunology |date=October 2003 |volume=3 |issue=5 |pages=337–342 |doi=10.1097/00130832-200310000-00003 |pmid=14501431 |s2cid=45020780 }}</ref> The hypothesis states that the vital microbial exposures are not colds, influenza, measles and other common childhood infections which have evolved relatively recently over the last 10,000 years, but rather the microbes already present during mammalian and human evolution, that could persist in small hunter-gatherer groups as microbiota, tolerated latent infections, or carrier states. He proposed that [[coevolution]] with these species has resulted in their gaining a role in immune system development.

Strachan's original formulation of the hygiene hypothesis also centred around the idea that smaller families provided insufficient microbial exposure partly because of less person-to-person spread of infections, but also because of "improved household amenities and higher standards of personal cleanliness".<ref name=strachan2000 /> It seems likely that this was the reason he named it the "hygiene hypothesis". Although the "hygiene revolution" of the nineteenth and twentieth centuries may have been a major factor, it now seems more likely that, although public health measures such as [[sanitation]], [[potable water]] and [[garbage collection]] were instrumental in reducing our exposure to [[cholera]], [[typhoid]] and so on, they also deprived people of their exposure to the "old friends" that occupy the same environmental habitats.<ref name=stanwellsmith>{{cite journal |first1=Rosalind Stanwell |last1=Smith |first2=Sally F. |last2=Bloomfield |first3=Graham A. |last3=Rook |title=The Hygiene Hypothesis and its implications for home hygiene, lifestyle and public health |journal=Home Hygiene & Health |date=September 2012 |url=https://www.ifh-homehygiene.org/review-best-practice/hygiene-hypothesis-and-its-implications-home-hygiene-lifestyle-and-public-0 }}</ref>

The rise of [[autoimmune disease]]s and [[acute lymphoblastic leukemia]] in young people in the developed world was linked to the hygiene hypothesis.<ref>{{cite journal |last1=Smith |first1=Malcolm A. |last2=Simon |first2=Richard |last3=Strickler |first3=Howard D. |last4=McQuillan |first4=Geraldine |last5=Gloeckler Ries |first5=Lynn A. |last6=Linet |first6=Martha S. |title=Evidence that childhood acute lymphoblastic leukemia is associated with an infectious agent linked to hygiene conditions |journal=Cancer Causes & Control |date=1998 |volume=9 |issue=3 |pages=285–298 |doi=10.1023/A:1008873103921 |pmid=9684709 |s2cid=25397922 }}</ref><ref name=Okada2010>{{cite journal |last1=Okada |first1=H. |last2=Kuhn |first2=C. |last3=Feillet |first3=H. |last4=Bach |first4=J.-F. |title=The 'hygiene hypothesis' for autoimmune and allergic diseases: an update |journal=Clinical & Experimental Immunology |date=11 March 2010 |volume=160 |issue=1 |pages=1–9 |doi=10.1111/j.1365-2249.2010.04139.x |pmid=20415844 |pmc=2841828 }}</ref><ref>{{cite journal |last1=Greaves |first1=Mel |title=A causal mechanism for childhood acute lymphoblastic leukaemia |journal=Nature Reviews Cancer |date=August 2018 |volume=18 |issue=8 |pages=471–484 |doi=10.1038/s41568-018-0015-6 |pmid=29784935 |pmc=6986894 }}</ref> [[Autism]] may be associated with changes in the gut microbiome and early infections.<ref>{{cite journal |last1=Vallès |first1=Yvonne |last2=Francino |first2=M. Pilar |title=Air Pollution, Early Life Microbiome, and Development |journal=Current Environmental Health Reports |date=29 September 2018 |volume=5 |issue=4 |pages=512–521 |doi=10.1007/s40572-018-0215-y |pmid=30269309 |pmc=6306492 }}</ref> The risk of chronic inflammatory diseases also depends on factors such as diet, pollution, physical activity, obesity, socio-economic factors and stress. Genetic predisposition is also a factor.<ref name= rockgaw /><ref name=filippi2008>{{cite journal |last1=Filippi |first1=C. M. |last2=von Herrath |first2=M. G. |title=Viral Trigger for Type 1 Diabetes: Pros and Cons |journal=Diabetes |date=29 October 2008 |volume=57 |issue=11 |pages=2863–2871 |doi=10.2337/db07-1023 |pmid=18971433 |pmc=2570378 }}</ref><ref name=rook2012>{{cite journal |last1=Rook |first1=Graham A. W. |title=Hygiene Hypothesis and Autoimmune Diseases |journal=Clinical Reviews in Allergy & Immunology |date=17 November 2011 |volume=42 |issue=1 |pages=5–15 |doi=10.1007/s12016-011-8285-8 |pmid=22090147 |s2cid=15302882 }}</ref>

== History ==

Since allergies and other chronic inflammatory diseases are largely diseases of the last 100 years or so, the "hygiene revolution" of the last 200 years came under scrutiny as a possible cause. During the 1800s, radical improvements to sanitation and water quality occurred in Europe and North America. The introduction of toilets and sewer systems and the cleanup of city streets, and cleaner food were part of this program. This in turn led to a rapid decline in infectious diseases, particularly during the period 1900–1950, through reduced exposure to infectious agents.<ref name=stanwellsmith />

Although the idea that exposure to certain infections may decrease the risk of allergy is not new, Strachan was one of the first to formally propose it, in an article published in the ''[[British Medical Journal]]'' in 1989. This article proposed to explain the observation that [[hay fever]] and [[eczema]], both allergic diseases, were less common in children from larger families, which were presumably exposed to more infectious agents through their siblings, than in children from families with only one child.<ref>{{cite journal |last1=Strachan |first1=D. P. |title=Hay fever, hygiene, and household size. |journal=BMJ |date=18 November 1989 |volume=299 |issue=6710 |pages=1259–1260 |doi=10.1136/bmj.299.6710.1259 |pmid=2513902 |pmc=1838109 }}</ref> The increased occurrence of allergies had previously been thought to be a result of increasing pollution.<ref name="Bjorksten2009"/> The hypothesis was extensively investigated by [[immunology|immunologists]] and [[epidemiology|epidemiologists]] and has become an important theoretical framework for the study of chronic inflammatory disorders.

The "old friends hypothesis" proposed in 2003<ref name=rook2003/> may offer a better explanation for the link between microbial exposure and inflammatory diseases.<ref name=rook2013/><ref name=rook2003/> This hypothesis argues that the vital exposures are not common cold and other recently evolved infections, which are no older than 10,000 years, but rather microbes already present in hunter-gatherer times when the human immune system was evolving. Conventional childhood infections are mostly "[[crowd infections]]" that kill or immunise and thus cannot persist in isolated hunter-gatherer groups. Crowd infections started to appear after the [[neolithic agriculture|neolithic agricultural]] revolution, when human populations increased in size and proximity. The microbes that co-evolved with mammalian immune systems are much more ancient. According to this hypothesis, humans became so dependent on them that their immune systems can neither develop nor function properly without them.

Rook proposed that these microbes most likely include:

* Ambient species that exist in the same environments as humans
* Species that inhabit human skin, gut and respiratory tract, and that of the animals we live with
* Organisms such as [[virus]]es and [[helminth]]s (worms) that establish chronic infections or carrier states that humans can tolerate and so could co-evolve a specific immunoregulatory relationship with the immune system.

The modified hypothesis later expanded to include exposure to [[symbiotic]] bacteria and parasites.<ref name=grammatikos2008>{{cite journal |last1=Grammatikos |first1=Alexandros P. |title=The genetic and environmental basis of atopic diseases |journal=Annals of Medicine |date=8 July 2009 |volume=40 |issue=7 |pages=482–495 |doi=10.1080/07853890802082096 |pmid=18608118 |s2cid=188280 }}</ref>

"Evolution turns the inevitable into a necessity." This means that the majority of mammalian evolution took place in mud and rotting vegetation and more than 90 percent of human evolution took place in isolated hunter-gatherer communities and farming communities. Therefore, the human immune systems have evolved to anticipate certain types of microbial input, making the inevitable exposure into a necessity. The organisms that are implicated in the hygiene hypothesis are not proven to cause the disease prevalence, however there are sufficient data on lactobacilli, saprophytic environment mycobacteria, and helminths and their association. These bacteria and parasites have commonly been found in vegetation, mud, and water throughout evolution.<ref name=rook2013/><ref name=rook2003/>

Multiple possible mechanisms have been proposed for how the 'Old Friends' microorganisms prevent autoimmune diseases and asthma. They include:
# Reciprocal inhibition between immune responses directed against distinct antigens of the Old Friends microbes which elicit stronger immune responses than the weaker autoantigens and allergens of autoimmune disease and allergy respectively.
# Competition for cytokines, MHC receptors and growth factors needed by the immune system to mount an immune response.
# Immunoregulatory interactions with host TLRs.<ref name=Okada2010/>

The "microbial diversity" hypothesis, proposed by Paolo Matricardi and developed by von Hertzen,<ref name=matricardi2010>{{cite journal |last1=Matricardi |first1=P. M. |title=99th Dahlem Conference on Infection, Inflammation and Chronic Inflammatory Disorders: Controversial aspects of the 'hygiene hypothesis' |journal=Clinical & Experimental Immunology |date=11 March 2010 |volume=160 |issue=1 |pages=98–105 |doi=10.1111/j.1365-2249.2010.04130.x |pmid=20415858 |pmc=2841842 }}</ref><ref name=vonhertzen2011>{{cite journal |last1=von Hertzen |first1=Leena |last2=Hanski |first2=Ilkka |last3=Haahtela |first3=Tari |title=Natural immunity |journal=EMBO Reports |date=7 October 2011 |volume=12 |issue=11 |pages=1089–1093 |doi=10.1038/embor.2011.195 |pmid=21979814 |pmc=3207110 }}</ref> holds that diversity of [[Gut flora|microbes in the gut]] and other sites is a key factor for priming the immune system, rather than stable colonization with a particular species. Exposure to diverse organisms in early development builds a "database" that allows the immune system to identify harmful agents and normalize once the danger is eliminated.

For allergic disease, the most important times for exposure are: early in development; later during pregnancy; and the first few days or months of infancy. Exposure needs to be maintained over a significant period. This fits with evidence that delivery by [[Caesarean section]] may be associated with increased allergies, whilst breastfeeding can be protective.<ref name=stanwellsmith />

== Evolution of the adaptive immune system ==

Humans and the microbes they harbor have co-evolved for thousands of centuries; however, it is thought that the human species has gone through numerous phases in history characterized by different pathogen exposures. For instance, in very early human societies, small interaction between its members has given particular selection to a relatively limited group of pathogens that had high transmission rates. It is considered that the human immune system is likely subjected to a selective pressure from pathogens that are responsible for down regulating certain alleles and therefore phenotypes in humans. The [[thalassemia]] genes that are shaped by the ''[[Plasmodium]]'' species expressing the selection pressure might be a model for this theory<ref>{{cite journal |last1=Vrushali |first1=Pathak |last2=Roshan |first2=Roshan |last3=Kanjaksha |first3=Ghosh |title=Plasmodium falciparum malaria skews globin gene expression balance in in-vitro haematopoietic stem cell culture system: Its implications in malaria associated anemia |journal=Exp. Parasitol. |date=Feb 2018 |volume=185 |pages=29–38 |doi=10.1016/j.exppara.2018.01.003 |pmid=29309785 }}</ref> but is not shown in-vivo.

Recent comparative genomic studies have shown that immune response genes (protein coding and non-coding regulatory genes) have less evolutionary constraint, and are rather more frequently targeted by positive selection from pathogens that coevolve with the human subject. Of all the various types of pathogens known to cause disease in humans, helminths warrant special attention, because of their ability to modify the prevalence or severity of certain immune-related responses in human and mouse models. In fact recent research has shown that parasitic worms have served as a stronger selective pressure on select human genes encoding interleukins and interleukin receptors when compared to viral and bacterial pathogens. Helminths are thought to have been as old as the [[adaptive immune system]], suggesting that they may have co-evolved, also implying that our immune system has been strongly focused on fighting off helminthic infections, insofar as to potentially interact with them early in infancy. The host-pathogen interaction is a very important relationship that serves to shape the immune system development early on in life.<ref>{{cite journal |last1=Sironi |first1=Manuela |last2=Clerici |first2=Mario |title=The hygiene hypothesis: an evolutionary perspective |journal=Microbes and Infection |date=June 2010 |volume=12 |issue=6 |pages=421–427 |doi=10.1016/j.micinf.2010.02.002 |pmid=20178858 }}</ref><ref>{{cite journal |last1=Wolfe |first1=Nathan D. |last2=Dunavan |first2=Claire Panosian |last3=Diamond |first3=Jared |title=Origins of major human infectious diseases |journal=Nature |date=May 2007 |volume=447 |issue=7142 |pages=279–283 |doi=10.1038/nature05775 |pmid=17507975 |bibcode=2007Natur.447..279W |pmc=7095142 }}</ref><ref>{{cite journal |last1=Kosiol |first1=Carolin |last2=Vinař |first2=Tomáš |last3=da Fonseca |first3=Rute R. |last4=Hubisz |first4=Melissa J. |last5=Bustamante |first5=Carlos D. |last6=Nielsen |first6=Rasmus |last7=Siepel |first7=Adam |last8=Schierup |first8=Mikkel H. |title=Patterns of Positive Selection in Six Mammalian Genomes |journal=PLOS Genetics |date=1 August 2008 |volume=4 |issue=8 |pages=e1000144 |doi=10.1371/journal.pgen.1000144 |pmid=18670650 |pmc=2483296 }}</ref><ref>{{cite journal |last1=Fumagalli |first1=Matteo |last2=Pozzoli |first2=Uberto |last3=Cagliani |first3=Rachele |last4=Comi |first4=Giacomo P. |last5=Riva |first5=Stefania |last6=Clerici |first6=Mario |last7=Bresolin |first7=Nereo |last8=Sironi |first8=Manuela |title=Parasites represent a major selective force for interleukin genes and shape the genetic predisposition to autoimmune conditions |journal=The Journal of Experimental Medicine |date=8 June 2009 |volume=206 |issue=6 |pages=1395–1408 |doi=10.1084/jem.20082779 |pmid=19468064 |pmc=2715056 }}</ref>

== Biological basis ==

The primary proposed mechanism of the hygiene hypothesis is an imbalance between the T<sub>H</sub>1 and T<sub>H</sub>2 subtypes of [[T helper cell]]s.<ref name="Haga2017"/><ref name="Leong2016"/> Insufficient activation of the T<sub>H</sub>1 arm would stimulate the cell defense of the immune system and lead to an overactive T<sub>H</sub>2 arm, stimulating the antibody-mediated immunity of the immune systems, which in turn led to allergic disease.<ref>{{cite journal |last1=Folkerts |first1=Gert |last2=Walzl |first2=Gerhard |last3=Openshaw |first3=Peter J.M. |title=Do common childhood infections 'teach' the immune system not to be allergic? |journal=Immunology Today |date=March 2000 |volume=21 |issue=3 |pages=118–120 |doi=10.1016/s0167-5699(00)01582-6 |pmid=10777250 }}</ref>

However, this explanation cannot explain the rise in incidence (similar to the rise of allergic diseases) of several T<sub>H</sub>1-mediated [[autoimmunity|autoimmune diseases]], including [[inflammatory bowel disease]], [[multiple sclerosis]] and [[Diabetes mellitus type 1|type I diabetes]]. [Figure 1Bach] However, the North South Gradient seen in the prevalence of multiple sclerosis has been found to be inversely related to the global distribution of parasitic infection.[Figure 2Bach] Additionally, research has shown that MS patients infected with parasites displayed T<sub>H</sub>2 type immune responses as opposed to the proinflammatory T<sub>H</sub>1 immune phenotype seen in non-infected multiple sclerosis patients.[Fleming] Parasite infection has also been shown to improve inflammatory bowel disease and may act in a similar fashion as it does in multiple sclerosis.[Lee]{{citation needed|date=April 2020}}

Allergic conditions are caused by inappropriate immunological responses to harmless [[antigens]] driven by a [[t helper cell|T<sub>H</sub>2]]-mediated immune response, T<sub>H</sub>2 cells produce [[interleukin 4]], [[interleukin 5]], [[interleukin 6]], [[interleukin 13]] and predominantly [[immunoglobulin E]].<ref name=Okada2010/> Many [[bacteria]] and [[virus]]es elicit a [[t helper cell|T<sub>H</sub>1]]-mediated immune response, which down-regulates T<sub>H</sub>2 responses. T<sub>H</sub>1 immune responses are characterized by the secretion of pro-inflammatory cytokines such as [[interleukin 2]], [[IFNγ]], and [[TNFα]]. Factors that favor a predominantly T<sub>H</sub>1 phenotype include: older siblings, large family size, early day care attendance, infection (TB, measles, or hepatitis), rural living, or contact with animals. A T<sub>H</sub>2-dominated phenotype is associated with high antibiotic use, western lifestyle, urban environment, diet, and sensitivity to dust mites and cockroaches. T<sub>H</sub>1 and T<sub>H</sub>2 responses are reciprocally inhibitory, so when one is active, the other is suppressed.<ref>{{cite journal |last1=Kramer |first1=A. |last2=Bekeschus |first2=S. |last3=Bröker |first3=B.M. |last4=Schleibinger |first4=H. |last5=Razavi |first5=B. |last6=Assadian |first6=O. |title=Maintaining health by balancing microbial exposure and prevention of infection: the hygiene hypothesis versus the hypothesis of early immune challenge |journal=Journal of Hospital Infection |date=February 2013 |volume=83 |pages=S29–S34 |doi=10.1016/S0195-6701(13)60007-9 |pmid=23453173 }}</ref><ref>{{cite journal |last1=Lee |first1=S. J. |last2=Maizels |first2=R. M. |title=Inflammatory Bowel Disease |journal=Evolution, Medicine, and Public Health |date=18 April 2014 |volume=2014 |issue=1 |pages=95 |doi=10.1093/emph/eou017 |pmid=24747119 |pmc=4204624 }}</ref><ref>{{cite journal |last1=Weinberg |first1=Eugene G. |title=Urbanization and childhood asthma: An African perspective |journal=Journal of Allergy and Clinical Immunology |date=February 2000 |volume=105 |issue=2 |pages=224–231 |doi=10.1016/s0091-6749(00)90069-1 |pmid=10669840 }}</ref>

An alternative explanation is that the developing immune system must receive stimuli (from infectious agents, symbiotic bacteria, or parasites) to adequately develop [[regulatory T cell]]s. Without that stimuli it becomes more susceptible to autoimmune diseases and allergic diseases, because of insufficiently repressed T<sub>H</sub>1 and T<sub>H</sub>2 responses, respectively.<ref>{{cite journal |last1=Bufford |first1=Jeremy D. |last2=Gern |first2=James E. |title=The Hygiene Hypothesis Revisited |journal=Immunology and Allergy Clinics of North America |date=May 2005 |volume=25 |issue=2 |pages=247–262 |doi=10.1016/j.iac.2005.03.005 |pmid=15878454 }}</ref> For example, all chronic inflammatory disorders show evidence of failed immunoregulation.<ref name=rockgaw>{{cite journal |last1=Rook |first1=G. A. W. |title=99th Dahlem Conference on Infection, Inflammation and Chronic Inflammatory Disorders: Darwinian medicine and the 'hygiene' or 'old friends' hypothesis |journal=Clinical & Experimental Immunology |date=11 March 2010 |volume=160 |issue=1 |pages=70–79 |doi=10.1111/j.1365-2249.2010.04133.x |pmid=20415854 |pmc=2841838 }}</ref> Secondly, helminths, non-pathogenic ambient pseudocommensal bacteria or certain gut [[commensal]]s and [[probiotics]], drive immunoregulation. They block or treat models of all chronic inflammatory conditions.<ref name=osada2010>{{cite journal |last1=Osada |first1=Yoshio |last2=Kanazawa |first2=Tamotsu |title=Parasitic Helminths: New Weapons against Immunological Disorders |journal=Journal of Biomedicine and Biotechnology |date=2010 |volume=2010 |pages=743758 |doi=10.1155/2010/743758 |pmid=20169100 |pmc=2821776 |doi-access=free }}</ref>

== Evidence ==

There is a significant amount of evidence supporting the idea that microbial exposure is linked to allergies or other conditions,<ref name="StiemsmaReynolds2015"/><ref name="Daley2014">{{cite journal |last1=Daley |first1=Denise |title=The evolution of the hygiene hypothesis |journal=Current Opinion in Allergy and Clinical Immunology |date=October 2014 |volume=14 |issue=5 |pages=390–396 |doi=10.1097/ACI.0000000000000101 |pmid=25102107 |s2cid=45420527 }}</ref><ref name="VersiniJeandel2015">{{cite journal |last1=Versini |first1=Mathilde |last2=Jeandel |first2=Pierre-Yves |last3=Bashi |first3=Tomer |last4=Bizzaro |first4=Giorgia |last5=Blank |first5=Miri |last6=Shoenfeld |first6=Yehuda |title=Unraveling the Hygiene Hypothesis of helminthes and autoimmunity: origins, pathophysiology, and clinical applications |journal=BMC Medicine |date=13 April 2015 |volume=13 |issue=1 |pages=81 |doi=10.1186/s12916-015-0306-7 |pmid=25879741 |pmc=4396177 }}</ref> although scientific disagreement still exists.<ref name="Silva2018"/><ref name="Bjorksten2009"/><ref name="Bernardes2017"/> Since hygiene is difficult to define or measure directly, surrogate markers are used such as socioeconomic status, income, and diet.<ref name="Leong2016"/>

Studies have shown that various immunological and autoimmune diseases are much less common in the developing world than the industrialized world and that immigrants to the industrialized world from the developing world increasingly develop immunological disorders in relation to the length of time since arrival in the industrialized world.<ref name=Okada2010/> This is true for asthma and other chronic inflammatory disorders.<ref name=rook2013 /> The increase in allergy rates is primarily attributed to diet and reduced microbiome diversity, although the mechanistic reasons are unclear.<ref name="LambrechtHammad2017">{{cite journal |last1=Lambrecht |first1=Bart N |last2=Hammad |first2=Hamida |title=The immunology of the allergy epidemic and the hygiene hypothesis |journal=Nature Immunology |date=1 October 2017 |volume=18 |issue=10 |pages=1076–1083 |doi=10.1038/ni.3829 |pmid=28926539 |s2cid=6239349 }}</ref>

The use of antibiotics in the first year of life has been linked to asthma and other allergic diseases,<ref>{{cite journal |last1=Marra |first1=Fawziah |last2=Lynd |first2=Larry |last3=Coombes |first3=Megan |last4=Richardson |first4=Kathryn |last5=Legal |first5=Michael |last6=FitzGerald |first6=J. Mark |last7=Marra |first7=Carlo A. |title=Does Antibiotic Exposure During Infancy Lead to Development of Asthma? |journal=Chest |date=March 2006 |volume=129 |issue=3 |pages=610–618 |doi=10.1378/chest.129.3.610 |pmid=16537858 }}</ref> and increased asthma rates are also associated with birth by [[Caesarean section]].<ref>{{cite journal |last1=Thavagnanam |first1=S. |last2=Fleming |first2=J. |last3=Bromley |first3=A. |last4=Shields |first4=M. D. |last5=Cardwell |first5=C. R. |title=A meta-analysis of the association between Caesarean section and childhood asthma |journal=Clinical & Experimental Allergy |date=April 2008 |volume=38 |issue=4 |pages=629–633 |doi=10.1111/j.1365-2222.2007.02780.x |pmid=18352976 |s2cid=23077809 }}</ref> However, at least one study suggests that personal hygienic practices may be unrelated to the incidence of asthma.<ref name="Bernardes2017"/> Antibiotic usage reduces the diversity of gut microbiota. Although several studies have shown associations between antibiotic use and later development of asthma or allergy, other studies suggest that the effect is due to more frequent antibiotic use in asthmatic children. Trends in vaccine use may also be relevant, but epidemiological studies provide no consistent support for a detrimental effect of vaccination/immunization on [[atopy]] rates.<ref name=stanwellsmith /> In support of the old friends hypothesis, the intestinal microbiome was found to differ between allergic and non-allergic Estonian and Swedish children (although this finding was not replicated in a larger cohort), and the biodiversity of the intestinal flora in patients with Crohn's disease was diminished.<ref name=Okada2010/>

===Limitations===

The hygiene hypothesis does not apply to all populations.<ref name="Bernardes2017"/><ref name="Leong2016"/> For example, in the case of [[inflammatory bowel disease]], it is primarily relevant when a person's level of affluence increases, either due to changes in society or by moving to a more affluent country, but not when affluence remains constant at a high level.<ref name="Leong2016">{{cite journal |last1=Leong |first1=Rupert W. |last2=Mitrev |first2=Nikola |last3=Ko |first3=Yanna |title=Hygiene Hypothesis: Is the Evidence the Same All Over the World? |journal=Digestive Diseases |date=2016 |volume=34 |issue=1–2 |pages=35–42 |doi=10.1159/000442922 |pmid=26982573 |s2cid=21373849 }}</ref>

The hygiene hypothesis has difficulty explaining why allergic diseases also occur in less affluent regions.<ref name="Bernardes2017"/> Additionally, exposure to some microbial species actually increases future susceptibility to disease instead, as in the case of infection with [[rhinovirus]] (the main source of the [[common cold]]) which increases the risk of asthma.<ref name="Silva2018"/><ref name="Haspeslagh2018">{{cite journal |last1=Haspeslagh |first1=Eline |last2=Heyndrickx |first2=Ines |last3=Hammad |first3=Hamida |last4=Lambrecht |first4=Bart N |title=The hygiene hypothesis: immunological mechanisms of airway tolerance |journal=Current Opinion in Immunology |date=October 2018 |volume=54 |pages=102–108 |doi=10.1016/j.coi.2018.06.007 |pmid=29986301 |pmc=6202673 |doi-access=free }}</ref>

== Treatment ==

Current research suggests that manipulating the intestinal microbiota may be able to treat or prevent allergies and other immune-related conditions.<ref name="StiemsmaReynolds2015"/> Various approaches are under investigation. [[Probiotic]]s (drinks or foods) have never been shown to reintroduce microbes to the gut. As yet, therapeutically relevant microbes have not been specifically identified.<ref name=sanders2013>{{cite journal |last1=Sanders |first1=Mary Ellen |last2=Guarner |first2=Francisco |last3=Guerrant |first3=Richard |last4=Holt |first4=Peter R |last5=Quigley |first5=Eamonn MM |last6=Sartor |first6=R Balfour |last7=Sherman |first7=Philip M |last8=Mayer |first8=Emeran A |title=An update on the use and investigation of probiotics in health and disease |journal=Gut |date=May 2013 |volume=62 |issue=5 |pages=787–796 |doi=10.1136/gutjnl-2012-302504 |pmid=23474420 |pmc=4351195 }}</ref> However, probiotic bacteria have been found to reduce allergic symptoms in some studies.<ref name="ShuYuen2018"/> Other approaches being researched include [[prebiotics]], which promote the growth of gut flora, and [[synbiotics]], the use of prebiotics and probiotics at the same time.<ref name="StiemsmaReynolds2015"/>

Should these therapies become accepted, public policy implications include providing green spaces in urban areas or even providing access to agricultural environments for children.<ref name="gaw in press">{{cite journal |last1=Rook |first1=G. A. |title=Regulation of the immune system by biodiversity from the natural environment: An ecosystem service essential to health |journal=Proceedings of the National Academy of Sciences |date=23 October 2013 |volume=110 |issue=46 |pages=18360–18367 |doi=10.1073/pnas.1313731110 |pmid=24154724 |pmc=3831972 |bibcode=2013PNAS..11018360R |doi-access=free }}</ref>

[[Helminthic therapy]] is the treatment of [[autoimmune disease]]s and [[immune disorder]]s by means of deliberate infestation with a [[helminth]] [[larva]] or [[Ovum|ova]]. Helminthic therapy emerged from the search for reasons why the incidence of immunological disorders and autoimmune diseases correlates with the level of industrial development.<ref>{{cite journal |doi=10.1111/j.1365-3024.2006.00879.x |title=Parasitic worms and inflammatory diseases |year=2006 |last1=Zaccone |first1=P. |last2=Fehervari |first2=Z. |last3=Phillips |first3=J. M. |last4=Dunne |first4=D. W. |last5=Cooke |first5=A. |journal=Parasite Immunology |volume=28 |issue=10 |pages=515–23 |pmid=16965287 |pmc=1618732}}</ref><ref name="pmid 14684567">{{cite journal |doi=10.1136/gut.53.1.7 |title=Helminths and harmony |year=2004 |last1=Weinstock |first1=J V |journal=Gut |volume=53 |pages=7–9 |pmid=14684567 |last2=Summers |first2=R |last3=Elliott |first3=DE |issue=1 |pmc=1773927}}</ref> The exact relationship between helminths and allergies is unclear, in part because studies tend to use different definitions and outcomes, and because of the wide variety among both helminth species and the populations they infect.<ref name="SantiagoNutman2016">{{cite journal |last1=Nutman |first1=Thomas B. |last2=Santiago |first2=Helton C. |title=Human Helminths and Allergic Disease: The Hygiene Hypothesis and Beyond |journal=The American Journal of Tropical Medicine and Hygiene |date=5 October 2016 |volume=95 |issue=4 |pages=746–753 |doi=10.4269/ajtmh.16-0348 |pmid=27573628 |pmc=5062766 }}</ref> The infections induce a type 2 immune response, which likely evolved in mammals as a result of such infections; chronic helminth infection has been linked with a reduced sensitivity in peripheral T cells, and several studies have found deworming to lead to an increase in allergic sensitivity.<ref name="LokeLim2015"/><ref name="MaizelsMcSorley2014"/> However, in some cases helminths and other parasites are a cause of developing allergies instead.<ref name="Silva2018"/> In addition, such infections are not themselves a treatment as they are [[Helminthiasis|a major disease burden]] and in fact they are one of the most important [[neglected disease]]s.<ref name="LokeLim2015">{{cite journal |last1=Loke |first1=P. |last2=Lim |first2=Y. A. L. |title=Helminths and the microbiota: parts of the hygiene hypothesis |journal=Parasite Immunology |date=June 2015 |volume=37 |issue=6 |pages=314–323 |doi=10.1111/pim.12193 |pmid=25869420 |pmc=4428757 }}</ref><ref name="MaizelsMcSorley2014"/> The development of drugs that mimic the effects without causing disease is in progress.<ref name="Silva2018"/>

== Public health ==

The reduction of public confidence in hygiene has significant possible consequences for public health.<ref name="BloomfieldRook2016">{{cite journal |last1=Bloomfield |first1=Sally F |last2=Rook |first2=Graham AW |last3=Scott |first3=Elizabeth A |last4=Shanahan |first4=Fergus |last5=Stanwell-Smith |first5=Rosalind |last6=Turner |first6=Paul |title=Time to abandon the hygiene hypothesis: new perspectives on allergic disease, the human microbiome, infectious disease prevention and the role of targeted hygiene |journal=Perspectives in Public Health |date=27 June 2016 |volume=136 |issue=4 |pages=213–224 |doi=10.1177/1757913916650225 |pmid=27354505 |pmc=4966430 }}</ref> Hygiene is essential for protecting vulnerable populations such as the elderly from infections, preventing the spread of [[antibiotic resistance]], and for combating [[emerging infectious diseases]] such as [[SARS]] and [[Ebola]].<ref name="BloomfieldRook2016"/>

The misunderstanding of the term "hygiene hypothesis" has resulted in unwarranted [[Anti-vaccination movement|opposition to vaccination]] as well as other important public health measures.”<ref name="Bjorksten2009"/> It has been suggested that public awareness of the initial form of the hygiene hypothesis has led to an increased disregard for hygiene in the home.<ref>{{cite journal |last1=Taché |first1=J. |last2=Carpentier |first2=B. |title=Hygiene in the home kitchen: Changes in behaviour and impact of key microbiological hazard control measures |journal=Food Control |date=January 2014 |volume=35 |issue=1 |pages=392–400 |doi=10.1016/j.foodcont.2013.07.026 }}</ref> The effective communication of science to the public has been hindered by the presentation of the hygiene hypothesis and other health-related information in the media.<ref name="BloomfieldRook2016"/>

===Cleanliness===
No evidence supports the idea that reducing modern practices of cleanliness and hygiene would have any impact on rates of chronic inflammatory and allergic disorders, but a significant amount of evidence that it would increase the risks of infectious diseases.<ref name=stanwellsmith/> The phrase "targeted hygiene" has been used in order to recognize the importance of hygiene in avoiding pathogens.<ref name=":0" />

If home and personal cleanliness contributes to reduced exposure to vital microbes, its role is likely to be small. The idea that homes can be made “sterile” through excessive cleanliness is implausible, and the evidence shows that after cleaning, microbes are quickly replaced by dust and air from outdoors, by shedding from the body and other living things, as well as from food.<ref name=stanwellsmith/><ref name=bloomfield2012>{{cite journal |first1=Sally F. |last1=Bloomfield |first2=Martin |last2=Exner |first3=Carlo |last3=Signorelli |first4=Kumar Jyoti |last4=Nath |first5=Elizabeth A |last5=Scott |title=The Chain of Infection Transmission in the Home and Everyday Life Settings, and the Role of Hygiene in Reducing the Risk of Infection |journal=Home Hygiene & Health |date=July 2012 |url=https://www.ifh-homehygiene.org/review/chain-infection-transmission-home-and-everyday-life-settings-and-role-hygiene-reducing-risk }}</ref><ref name=isf>{{cite journal |first1=Sally F. |last1=Bloomfield |first2=Martin |last2=Exner |first3=Gaetano M |last3=Fara |first4=Kumar Jyoti |last4=Nath |first5=Elizabeth A |last5=Scott |title=Hygiene procedures in the home and their effectiveness: a review of the scientific evidence base |journal=Home Hygiene & Health |date=October 2013 |url=http://www.ifh-homehygiene.org/best-practice-review/hygiene-procedures-home-and-their-effectiveness-review-scientific-evidence-base }}</ref><ref name="Ege2017">{{cite journal |last1=Ege |first1=Markus J. |title=The Hygiene Hypothesis in the Age of the Microbiome |journal=Annals of the American Thoracic Society |date=November 2017 |volume=14 |issue=Supplement_5 |pages=S348–S353 |doi=10.1513/AnnalsATS.201702-139AW |pmid=29161087 }}</ref> The key point may be that the microbial content of urban housing has altered, not because of home and personal hygiene habits, but because they are part of urban environments. Diet and lifestyle changes also affects the gut, skin and respiratory microbiota.

At the same time that concerns about allergies and other chronic inflammatory diseases have been increasing, so also have concerns about infectious disease.<ref name=stanwellsmith /><ref name=bloomfield2009>{{cite journal |first1=Sally F. |last1=Bloomfield |first2=Martin |last2=Exner |first3=Gaetano M |last3=Fara |first4=Kumar Jyoti |last4=Nath |first5=Elizabeth A |last5=Scott |first6=Carolien Van der |last6=Voorden |title=The global burden of hygiene-related diseases in relation to the home and community |journal=Home Hygiene & Health |date=June 2009 |url=https://www.ifh-homehygiene.org/review/global-burden-hygiene-related-diseases-relation-home-and-community }}</ref><ref name=Bloomfield2013>{{cite journal |last1=Bloomfield |first1=Sally F. |last2=Scott |first2=Elizabeth A. |title=A risk assessment approach to use of antimicrobials in the home to prevent spread of infection |journal=American Journal of Infection Control |date=May 2013 |volume=41 |issue=5 |pages=S87–S93 |doi=10.1016/j.ajic.2013.01.001 |pmid=23622757 }}</ref> Infectious diseases continue to exert a heavy health toll. Preventing [[pandemics]] and reducing [[antibiotic resistance]] are global priorities, and hygiene is a cornerstone of containing these threats.

=== Infection risk management ===

The International Scientific Forum on Home Hygiene has developed a risk management approach to reducing home infection risks. This approach uses microbiological and epidemiological evidence to identify the key routes of infection transmission in the home. These data indicate that the critical routes involve the hands, hand and food contact surfaces and cleaning utensils. Clothing and household linens involve somewhat lower risks. Surfaces that contact the body, such as baths and hand basins, can act as infection vehicles, as can surfaces associated with toilets. Airborne transmission can be important for some pathogens. A key aspect of this approach is that it maximises protection against pathogens and infection, but is more relaxed about visible cleanliness in order to sustain normal exposure to other human, animal and environmental microbes.<ref name= bloomfield2012/>

== See also ==
* [[Antibacterial soap]]
* [[Diseases of affluence]]
* [[Germ theory of disease]]
* [[Helminthic therapy]] (includes more discussion of hygiene hypothesis)
* [[Hookworm]]
* [[Microbiomes of the built environment]]
* [[Vaginal seeding]]

== References ==
{{Reflist|30em}}

== Further reading ==
* {{cite book |last=Dunn |first=Rob |title=Never Home Alone: From Microbes to Millipedes, Camel Crickets, and Honeybees, the Natural History of Where We Live |year=2018 |publisher=Basic Books |isbn=978-1541645769}}
* {{cite book |title=Let Them Eat Dirt |year=2016 |last1=Finlay |first1=B. Brett |first2=Marie-Claire |last2=Arrieta |publisher=Algonquin Books |isbn=978-1616207380}}
* {{cite journal |last1=Hadley |first1=Caroline |title=Should auld acquaintance be forgot… |journal=EMBO Reports |date=December 2004 |volume=5 |issue=12 |pages=1122–1124 |doi=10.1038/sj.embor.7400308 |pmid=15577925 |pmc=1299202 }}
* {{cite journal |last1=Rook |first1=G A W |last2=Brunet |first2=LR |title=Microbes, immunoregulation, and the gut |journal=Gut |date=1 March 2005 |volume=54 |issue=3 |pages=317–320 |doi=10.1136/gut.2004.053785 |pmid=15710972 |pmc=1774411 }}
* {{cite journal |last1=Rook |first1=G. A. W. |last2=Adams |first2=V. |last3=Palmer |first3=R. |last4=Brunet |first4=L. Rosa |last5=Hunt |first5=J. |last6=Martinelli |first6=R. |title=Mycobacteria and other environmental organisms as immunomodulators for immunoregulatory disorders |journal=Springer Seminars in Immunopathology |date=1 February 2004 |volume=25 |issue=3–4 |pages=237–255 |doi=10.1007/s00281-003-0148-9 |pmid=15007629 |s2cid=11393930 }}

{{Portal bar|Biology|Medicine}}
{{Authority control}}

{{DEFAULTSORT:Hygiene Hypothesis}}
[[Category:Allergology]]
[[Category:Epidemiology]]
[[Category:Biological hypotheses]]
[[Category:Immunology theories]]

Version vom 31. März 2022, 08:34 Uhr

In der Medizin besagt die Hygienehypothese, dass die frühkindliche Exposition gegenüber bestimmten Mikroorganismen (wie der Darmflora und Helminthenparasiten) vor allergischen Erkrankungen schützt, indem sie zur Entwicklung des Immunsystems beitragen.[1][2] Insbesondere wird angenommen, dass eine mangelnde Exposition zu Defekten bei der Etablierung der Immuntoleranz führt. Der Zeitraum für die Exposition beginnt in utero und endet im Schulalter.[3]

Während sich frühe Versionen der Hypothese auf die Exposition gegenüber Mikroben im Allgemeinen bezogen, gelten aktualisierte Versionen für eine bestimmte Gruppe mikrobieller Arten, die sich gemeinsam mit dem Menschen entwickelt haben.[1][2][4] Die Aktualisierungen wurden mit verschiedenen Namen versehen, darunter die Hypothese des Mikrobiommangels, die Mikroflora-Hypothese und die Hypothese der „alten Freunde“.[4][5] Es gibt eine beträchtliche Menge an Beweisen, die die Idee stützen, dass die mangelnde Exposition gegenüber diesen Mikroben mit Allergien oder anderen Erkrankungen zusammenhängt[2][6][7], obwohl es immer noch wissenschaftliche Meinungsverschiedenheiten gibt.[4][8][9]

Der Begriff Hygienehypothese wurde als falsche Bezeichnung beschrieben, weil die Leute ihn fälschlicherweise so interpretieren, dass er sich auf persönliche Sauberkeit bezieht.[1][8][10][11] Es wird erwartet, dass die Reduzierung der persönlichen Hygiene, wie z. B. das Nichtwaschen der Hände vor dem Essen, einfach das Infektionsrisiko erhöht, ohne Auswirkungen auf Allergien oder Immunstörungen zu haben.[1][8][9] Hygiene ist unerlässlich, um gefährdete Bevölkerungsgruppen wie ältere Menschen vor Infektionen zu schützen, die Ausbreitung von Antibiotikaresistenzen zu verhindern und neu auftretende Infektionskrankheiten wie Ebola oder COVID-19 zu bekämpfen.[12] Die Hygienehypothese deutet nicht darauf hin, dass mehr Infektionen während der Kindheit ein Gesamtnutzen wären.[1][8]

Siehe auch

Literatur

Einzelnachweise

  1. ↑ a b c d e Megan Scudellari: News Feature: Cleaning up the hygiene hypothesis. In: Proceedings of the National Academy of Sciences of the United States of America. Band 114, Nr. 7, 14. Februar 2017, ISSN 1091-6490, S. 1433–1436, doi:10.1073/pnas.1700688114, PMID 28196925, PMC 5320962 (freier Volltext) – (nih.gov [abgerufen am 31. März 2022]).
  2. ↑ a b c Leah T. Stiemsma, Lisa A. Reynolds, Stuart E. Turvey, B. Brett Finlay: The hygiene hypothesis: current perspectives and future therapies. In: ImmunoTargets and Therapy. Band 4, 2015, ISSN 2253-1556, S. 143–157, doi:10.2147/ITT.S61528, PMID 27471720, PMC 4918254 (freier Volltext) – (nih.gov [abgerufen am 31. März 2022]).
  3. ↑ Caroline Roduit, Remo Frei, Erika von Mutius, Roger Lauener: The Hygiene Hypothesis. In: Environmental Influences on the Immune System. Springer, Vienna 2016, ISBN 978-3-7091-1890-0, S. 77–96, doi:10.1007/978-3-7091-1890-0_4.
  4. ↑ a b c Gabriel M. Alexandre-Silva, Pablo A. Brito-Souza, Ana C. S. Oliveira, Felipe A. Cerni, Umberto Zottich: The hygiene hypothesis at a glance: Early exposures, immune mechanism and novel therapies. In: Acta Tropica. Band 188, Dezember 2018, ISSN 1873-6254, S. 16–26, doi:10.1016/j.actatropica.2018.08.032, PMID 30165069 (nih.gov [abgerufen am 31. März 2022]).
  5. ↑ Reconstituting the depleted biome to prevent immune disorders. 13. Oktober 2010, abgerufen am 31. März 2022 (amerikanisches Englisch).
  6. ↑ D. Daley: The evolution of the hygiene hypothesis: the role of early-life exposures to viruses and microbes and their relationship to asthma and allergic diseases. In: Current opinion in allergy and clinical immunology. 2014, doi:10.1097/ACI.0000000000000101 (semanticscholar.org [abgerufen am 31. März 2022]).
  7. ↑ Mathilde Versini, Pierre-Yves Jeandel, Tomer Bashi, Giorgia Bizzaro, Miri Blank: Unraveling the Hygiene Hypothesis of helminthes and autoimmunity: origins, pathophysiology, and clinical applications. In: BMC medicine. Band 13, 13. April 2015, ISSN 1741-7015, S. 81, doi:10.1186/s12916-015-0306-7, PMID 25879741, PMC 4396177 (freier Volltext) – (nih.gov [abgerufen am 31. März 2022]).
  8. ↑ a b c d Bengt Björkstén: The hygiene hypothesis: do we still believe in it? In: Nestle Nutrition Workshop Series. Paediatric Programme. Band 64, 2009, ISSN 1661-6677, S. 11–18; discussion 18–22, 251–257, doi:10.1159/000235780, PMID 19710512 (nih.gov [abgerufen am 31. März 2022]).
  9. ↑ a b Erik van Tilburg Bernardes, Marie-Claire Arrieta: Hygiene Hypothesis in Asthma Development: Is Hygiene to Blame? In: Archives of Medical Research. Band 48, Nr. 8, November 2017, ISSN 1873-5487, S. 717–726, doi:10.1016/j.arcmed.2017.11.009, PMID 29224909 (nih.gov [abgerufen am 31. März 2022]).
  10. ↑ M. Wendel-Haga, E. G. Celius: Is the hygiene hypothesis relevant for the risk of multiple sclerosis? In: Acta Neurologica Scandinavica. 136 Suppl 201, November 2017, ISSN 1600-0404, S. 26–30, doi:10.1111/ane.12844, PMID 29068485 (nih.gov [abgerufen am 31. März 2022]).
  11. ↑ William Parker: The “hygiene hypothesis” for allergic disease is a misnomer. In: BMJ : British Medical Journal. 2014, doi:10.1136/bmj.g5267 (semanticscholar.org [abgerufen am 31. März 2022]).
  12. ↑ Sally F. Bloomfield, Graham Aw Rook, Elizabeth A. Scott, Fergus Shanahan, Rosalind Stanwell-Smith: Time to abandon the hygiene hypothesis: new perspectives on allergic disease, the human microbiome, infectious disease prevention and the role of targeted hygiene. In: Perspectives in Public Health. Band 136, Nr. 4, Juli 2016, ISSN 1757-9147, S. 213–224, doi:10.1177/1757913916650225, PMID 27354505, PMC 4966430 (freier Volltext) – (nih.gov [abgerufen am 31. März 2022]).
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