Abstract:
: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.
journal_name
Virologyjournal_title
Virologyauthors
Anderson VE,Nguyen Y,Weinberg JBdoi
10.1016/j.virol.2009.06.009subject
Has Abstractpub_date
2009-08-15 00:00:00pages
25-32issue
1eissn
0042-6822issn
1096-0341pii
S0042-6822(09)00347-Xjournal_volume
391pub_type
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