Background: Atopic diseases, including asthma, have increased to epidemic proportions in the westernized world. The reasons for this increase are not known, nor are the mechanisms behind the development of these diseases. An interesting aspect of atopic disease is the role of respiratory viruses in the development of asthma and atopy. In fact, severe respiratory viral infection in infancy has been associated with a greatly increased risk of asthma.
Objective: This paper explores potential mechanisms through which viruses impart an increased risk of asthma, focusing on new pathways in mouse models of atopy.
Methods: A search of MEDLINE (1950-March 2008) was conducted using terms that included viral-induced wheeze, respiratory virus, asthma, IgE, and dendritic cells.
Results: A total of 1643 publications were identified that contained > or = 1 of the search terms; however, only 7 of these focused on immunoglobulin E (IgE) and the viral risk of asthma, and only 1 of the 7 explored the role of dendritic cells in this process. The latter study suggested a mechanistic link between lung dendritic cells and the development of postviral atopic disease. Important in this pathway is the generation of IgE, its high-affinity receptor, and the T-cell chemoattractant CCL28.
Conclusions: Data from recent mouse models suggest that the development of asthma after severe respiratory viral infection may be the result of a response generated by production of antiviral IgE, which is capable of engaging dendritic cells to form a chemoattractant for interleukin-13-producing T cells. This new paradigm points to a focus for development of future therapies to prevent or at least ameliorate post- viral atopic disease.