Hygiene hypothesis
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In medicine, the hygiene hypothesis states that a lack of early childhood exposure to infectious agents increases susceptibility to allergic diseases [1].
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[edit] Overview
First proposed by David P. Strachan in an article published in the British Medical Journal (now BMJ), in 1989 [2], the hygiene hypothesis was developed 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. The hygiene hypothesis has been extensively investigated by immunologists and epidemiologists and has become an important theoretical framework for the study of allergic disorders. Despite this, the infectious microorganisms or infectious microorganism-components believed to be responsible for these effects have yet to be identified and incorporated into medical practice and the contribution of hygiene levels to the rise of allergic disease has yet to be established[3].
[edit] Mechanism of Action
Allergic diseases are caused by inappropriate immunological responses to innocuous antigens driven by a TH2 type of immune response. Many bacteria and viruses elicit a TH1 type of immune response which has the ability to down-regulate the mediators of TH2 responses. These observations lead to the development of the first proposed mechanism of action of the hygiene hypothesis which stated that insufficient stimulation of the TH1 arm of the immune system lead to an overactive TH2 arm which in turn led to allergic disease [4].
This proposed mechanistic explanation fell out of favor because it cannot be easily reconciled with the fact that the incidence of inflammatory bowel disease (IBD), multiple sclerosis (MS), and type I diabetes, autoimmune diseases which are linked with an overactive TH1 type of immune response, is increasing in the same populations that are seeing increased allergic disease. The alternative mechanism which was eventually proposed addresses this shortcoming by hypothesizing that the developing immune system, if it does not receive stimuli from infectious agents, fails to properly develop cells with a regulatory function. A person lacking these cells is then more likely to develop autoimmune diseases because of insufficiently repressed TH1 reactions and allergic diseases due to insufficiently repressed TH2 immune reactions[5].
[edit] References
- ^ Strachan DP. Family size, infection and atopy: the first decade of the "hygiene hypothesis". Thorax 55 Suppl 1:S2-10.: S2-10, 2000.
- ^ Strachan DP. Hay fever, hygiene, and household size. BMJ 299: 1259-1260, 1989.
- ^ Schaub B, Lauener R and von ME. The many faces of the hygiene hypothesis. J Allergy Clin Immunol 117: 969-977, 2006.
- ^ Folkerts G, Walzl G, Openshaw PJ. Do common childhood infections 'teach' the immune system not to be allergic? Immunol Today 2000; 21(3):118-120.
- ^ Guarner F, Bourdet-Sicard R, Brandtzaeg P, Gill HS, McGuirk P, van EW, Versalovic J, Weinstock JV and Rook GA. Mechanisms of disease: the hygiene hypothesis revisited. Nat Clin Pract Gastroenterol Hepatol 3: 275-284, 2006.
[edit] Additional References
1. Camateros P, Moisan J, Henault J, De SJ, Skamene E and Radzioch D. Toll-like receptors, cytokines and the immunotherapeutics of asthma. Curr Pharm Des 12: 2365-2374, 2006.
