Inflammatory infiltration of the upper airway epithelium during Sendai virus infection: involvement of epithelial dendritic cells.

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We undertook the present study to determine the nature of the cellular inflammatory response within the epithelial lining of the rat trachea during a Sendai virus infection. In particular, we aimed to investigate changes in the resident population of epithelial dendritic cells. Rats were infected with Sendai virus, and tracheal tissue was examined immunohistochemically at various times with a panel of cell-specific monoclonal antibodies. We found that Sendai virus infection was restricted to only the lumenal layer of epithelial cells and that virus nucleoprotein was present from days 2 to 5 postinfection. Starting around day 2 or 3, there was a large cellular influx consisting of macrophages, neutrophils, NK cells, and T cells; this coincided with expression of high levels of ICAM-1 on the basal (uninfected) layers of the epithelium. The T cells were mostly alphabeta T-cell receptor positive; however, a smaller influx of gammadelta T cells also took place. The number of resident dendritic cells increased markedly during infection, with numbers peaking around day 5 and remaining elevated 14 days later. The peak of the inflammatory response occurred on day 5 and declined thereafter, with the exception of dendritic cell and alphabeta T-cell numbers, which remained elevated. Starting around day 3, the tracheal epithelial cells expressed increasing levels of major histocompatibility complex class II antigen. This expression was maximal at day 5 and declined rapidly thereafter. In vitro culture of tracheal segments demonstrated that viral infection was not per se responsible for the upregulation of class II expression and that when cultured in the presence of gamma interferon, class II antigen was induced on epithelial cells.

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