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• The hygiene hypothesis revisited
  Wendy J Anderson
  Published on: 8 March 2006

• Published on: 8 March 2006

  The hygiene hypothesis revisited

  • Wendy J Anderson, Consultant in Respiratory and General Medicine
  • Other Contributors:
    • Claire Butler, Graeme P Currie

  Dear Editor,

  The editorial by Cullinan suggests that the relationship between allergy, birth order and family size may not be completely explained by the hygiene hypothesis.[1] A role for infection in protecting against allergy has been under consideration for some years, although a credible mechanism has not been identified. It has been suggested that reduced exposure to infection in childhood shifted the balanc...

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  Dear Editor,

  The editorial by Cullinan suggests that the relationship between allergy, birth order and family size may not be completely explained by the hygiene hypothesis.[1] A role for infection in protecting against allergy has been under consideration for some years, although a credible mechanism has not been identified. It has been suggested that reduced exposure to infection in childhood shifted the balance between Th1 and Th2 cells in the adult immune system in favour of allergy associated Th2 cells.[2] This hypothesis failed to take account of the similarities in epidemiology of Th1 type I diabetes and Th2 mediated allergic disease, and while the role of infection was not challenged, the idea of Th2 dominated adult immune system was rejected.3 Cullinan suggests that the effect of birth order may be explained by differences in the intra uterine environment or by some alternative, non-infective aetiology. If future explanations are to have credibility, they require to take account of all the available evidence. It is difficult to explain the higher prevalence of Th1 and Th2 mediated disease in western societies and the more direct evidence that exposure to a variety of infections is protective on the basis of a non-infective cause.[2, 4-5]

  The control of any immune response involves mechanisms which may amplify or dampen the response. It seems likely that the presence of an immune response to one infection may non-specifically down regulate other immune responses, including allergic and autoimmune responses. The mechanism of down regulation remains to be identified but a unifying explanation which does not include infection seems implausible.

  References

  1. P Cullinan P. Childhood allergies, birth order and family size. Thorax 2006; 61: 3-5.

  2. Martinez F, Holt P. Role of microbial burdan in the aetiology of allergy and asthma. Lancet 1999;354(Suppl 2):12-15.

  3. Simpson C, Anderson W, Helms P, Taylor M, Watson L, Prescott G, et al. Coincidence of immune-mediated diseases driven by Th1 and Th2 subsets suggests a common aetiology. Clinical and experimental allergy 2002;2002:37-42.

  4. Lynch N, Hagel I, Perez M, prisco MD, R RL, Alvarez N. Effect of antihelminitic treatment on the allergic reactivity of children in a tropical slum. Journal of Allergy and Clinical Immunology. 1993;92:404- 11.

  5. Shirakawa T, Enomoto T, Shimazu S, JM. JH. The inverse association between tuberculin responses and atopic disorder. Science 1997;275:77-9.

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  Conflict of Interest:
  None declared.

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