Puzzling associations between childhood infections and the later occurrence of asthma and atopy

Ann Med. 2000 Sep;32(6):397-400. doi: 10.3109/07853890008995946.


The current unfavourable trends in asthma and atopy prevalences have raised great concern and have challenged investigators to accelerate search for new risk factors for atopic diseases. The lack or scarcity of intense, systemic infections in early life has been postulated to increase susceptibility of becoming sensitized to otherwise harmless allergens in later life. This hygiene hypothesis is considered one of the most plausible explanations for the current trends in atopic diseases to date. There are data to suggest that measles, hepatitis A, and Mycobacterium tuberculosis infection in early life may prevent the subsequent development of atopic diseases. The hypothesis is based on the concept that certain viral and bacterial infections, which induce a strongly polarized T helper (Th)-1 type response and a long-lasting memory immunity, are in early life able to reverse or prevent the biased Th1/Th2 balance in individuals prone to atopy and asthma. Evidence for the ability of mycobacterial infections to alter the Th1/Th2 balance has also been obtained from murine models. In humans, the critical time period during which immunomodulation with long-lasting effects is considered most successful is within the first two years of life. Possibly also nonpathogenic residents of the intestinal mucosa are involved in the proper maturation of the immune system. The use of antibiotics has been shown to be positively associated with the development of asthma and atopy. The mechanisms underlying these associations remain largely unknown.

Publication types

  • Review

MeSH terms

  • Anti-Bacterial Agents / therapeutic use
  • Asthma / epidemiology
  • Asthma / immunology*
  • Humans
  • Hypersensitivity, Immediate / epidemiology
  • Hypersensitivity, Immediate / immunology*
  • Immunologic Memory / physiology*
  • Infections / immunology*
  • Prevalence
  • Risk Factors
  • Th1 Cells / physiology*
  • Th2 Cells / physiology*
  • Time Factors


  • Anti-Bacterial Agents