Effects of allergic airway disease on mouse adenovirus type 1 respiratory infection

Virus infection may contribute to asthma pathogenesis. In turn, a Th2-polarized pulmonary environment may increase host susceptibility to infection. We used a cockroach antigen (CRA) model of allergic airway disease to test the hypothesis that Th2 cytokine overproduction increases susceptibility to mouse adenovirus type 1 (MAV-1). CRA sensitization led to upregulated lung expression of IL-4 and IL-13, lung cellular inflammation, and exaggerated airway mucus production. Following intranasal MAV-1 infection, lung cellular inflammation was more pronounced in CRA-sensitized mice than in unsensitized mice at 7 days post-infection but not at a later time point. CRA sensitization did not significantly suppress lung IFN-gamma expression, and lung IFN-gamma expression was upregulated in both CRA-sensitized mice and unsensitized mice over the course of MAV-1 infection. Despite CRA-induced differences in pulmonary inflammation, MAV-1 viral loads in lung and spleen and MAV-1 gene expression in the lung did not differ between CRA-sensitized and unsensitized mice. Our data therefore suggest that MAV-1 pathogenesis is not affected directly or indirectly by the Th2 polarization associated with allergic airway disease.