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This article is part of the supplement: Proceedings of the 6th Workshop on Animal Models of Asthma

Open AccessReview

Interaction of allergic airway inflammation and innate immunity: hygiene and beyond

Christoph Beisswenger1 email and Robert Bals2 email

1Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA

2Department of Internal Medicine, Division for Pulmonary Diseases, Philipps-Universtät Marburg, 35043 Marburg, Germany

author email corresponding author email

Journal of Occupational Medicine and Toxicology 2008, 3(Suppl 1):S3doi:10.1186/1745-6673-3-S1-S3

Published: 27 February 2008

Abstract

The lung is constantly exposed to the environment and its microbial components. Infections of the respiratory tract are amongst the most common diseases. Several concepts describe how this microbial exposure interacts with allergic airway disease as it is found in patients with asthma. Infections are classical triggers of asthma exacerbations. In contrast, the hygiene hypothesis offers an explanation for the increase in allergic diseases by establishing a connection between microbial exposure during childhood and the risk of developing asthma. This premise states that the microbial environment interacts with the innate immune system and that this interrelation is needed for the fine-tuning of the overall immune response. Based on the observed protective effect of farming environments against asthma, animal models have been developed to determine the effect of specific bacterial stimuli on the development of allergic inflammation. A variety of studies have shown a protective effect of bacterial products in allergen-induced lung inflammation. Conversely, recent studies have also shown that allergic inflammation inhibits antimicrobial host defense and renders animals more susceptible to bacterial infections. This paper focuses on examples of animal models of allergic disease that deal with the complex interactions of the innate and adaptive immune system and microbial stressors.


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