IL- 17 contributes to neutrophil recruitment but not to control of viral replication during acute mouse adenovirus type 1 respiratory infection
2014
McCarthy, Mary K. | Zhu, Lingqiao | Procario, Megan C. | Weinberg, Jason B.
IL-17-producing CD4⁺ helper T cells (Th17 cells) promote inflammatory responses to many pathogens. We used mouse adenovirus type 1 (MAV-1) to determine contributions of IL-17 to adenovirus pathogenesis. MAV-1 infection of C57BL/6 mice upregulated lung expression of IL-17 and the Th17-associated factors IL-23 and RORγt. Only CD4⁺T cells were associated with virus-specific IL-17 production. Fewer neutrophils were recruited to airways of IL-17⁻/⁻ mice following MAV-1 infection, but there were no other differences in pulmonary inflammation between IL-17⁺/⁺ and IL-17⁻/⁻ mice. Mice depleted of neutrophils using anti-Gr-1 antibody had greater lung viral loads than controls. Despite impaired neutrophil recruitment, there were no differences between IL-17⁺/⁺ and IL-17⁻/⁻ mice in peak lung viral loads, clearance of virus from the lungs, or establishment of protective immunity. We demonstrate robust Th17 responses during MAV-1 respiratory infection, but these responses are not essential for control of virus infection or for virus-induced pulmonary inflammation.
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