Abstract
Abstract Asthma is a chronic inflammatory disease of the airways characterized by a heightened response to normally harmless antigens. Respiratory Syncytial Virus (RSV) infections in children have been associated with predisposition to asthma in later life. However, the underlying molecular mechanisms are not well understood. RSV infection was recently shown to induce Th2 type cytokines such as IL-13 within 6 days after infection. Given this early induction of IL-13, we hypothesized that the source of RSV-induced IL-13 is a cell of the innate immune system. Our ongoing studies show rapid induction of alternatively activated macrophages (AAMs) in the lung following RSV infection. RSV induces expression of Arginase I (Arg I), a characteristic marker of AAMs and stimulates secretion of the Th2 cytokines IL-5 and IL-13 from the alveolar macrophages as early as 48 hours after infection. This was found to continue on day 5 after infection, being detectable in the lung tissue as well. These observations suggest that RSV, directly or indirectly, alters gene expression in alveolar macrophages very early after infection, which we hypothesize plays an important role in promoting an allergic immune response in the infected lungs.
Published Version
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