Prostaglandin E2 production during neonatal respiratory infection with mouse adenovirus type 1.

Neonatal mice are more susceptible than adults to mouse adenovirus type 1 (MAV1) respiratory infection. In adult mice, MAV-1 respiratory infection induces production of prostaglandin E 2 (PGE 2 ), a lipid mediator that exerts suppressive effects on a variety of host immune functions. We tested the hypothesis that exaggerated PGE 2 production in neonatal mice contributes to increased susceptibility to MAV-1. PGE 2 concentrations were lower in lungs of uninfected neonatal mice than in adults. PGE 2 production was induced by both MAV-1 and a nonspecific stimulus to a greater degree in neonatal mice than in adults, but only in adults was PGE 2 induced in a virus-specific manner. Lung viral loads were equivalent in PGE 2 -deficient neonatal mice and wild type controls, as was virus-induced expression of IFN-γ, IL-17A, and CCL5 in the lungs. PGE 2 deficiency had minimal effect on production of virus-specific IgG or establishment of protective immunity in neonatal mice. Collectively, our data indicate that lung PGE 2 production is exaggerated early in life, but this effect does not mediate increased susceptibility to MAV-1 infection. [ABSTRACT FROM AUTHOR]

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