Endotoxin exposure in allergy and asthma: reconciling a paradox

J Allergy Clin Immunol. 2002 Mar;109(3):379-92. doi: 10.1067/mai.2002.122157.


Well-established evidence links endotoxin exposure, especially in the workplace, to airways disease. Endotoxin can increase disease severity by acting as a natural adjuvant to augment asthma and atopic inflammation. Recent studies suggest that it can even act on its own, causing a distinct endotoxic form of asthma. Other studies, however, contradict the paradigm that endotoxin's influence is solely a negative one. Epidemiologic associations of environmental endotoxin exposure with allergy and asthma prevention are consistent with hygiene hypothesis associations of other microbial exposures or infections with a lower incidence of atopic disease. Currently, microbe-derived products are being developed as potential therapies for allergy and asthma. Thus it is an ideal time to consider endotoxin as a prototype of a natural intervention with microbial components. Nature's ongoing experiment with endotoxin can provide clues for the development of effective and safe microbe-based products for disease treatment and prevention. This article will discuss (1) conventional paradigms in which endotoxin-induced immune modulation by T(H)1-type induction leads to mitigation of T(H)2-type immune development, allergen sensitization, and atopic inflammation; (2) newer concepts of T(H)1-type immune responses that may provide additional asthma-protective effects by preventing airways remodeling; (3) home and environmental features that significantly contribute to endotoxin exposure; (4) different aspects of asthma mediated by endotoxin exposure; and (5) how to understand endotoxin's paradoxical nature of serving as both friend and foe.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Asthma* / etiology
  • Asthma* / immunology
  • Bacterial Infections / immunology
  • Child
  • Endotoxins* / adverse effects
  • Endotoxins* / immunology
  • Humans
  • Hypersensitivity* / etiology
  • Hypersensitivity* / immunology
  • Lipopolysaccharides / adverse effects
  • Lipopolysaccharides / immunology
  • Th1 Cells / immunology


  • Endotoxins
  • Lipopolysaccharides