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Wando Mount Pleasant Library
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IL-17 contributes to neutrophil recruitment but not to control of viral replication during acute mouse adenovirus type 1 respiratory infection.
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- Author(s): McCarthy, Mary K.1 ; Zhu, Lingqiao1 ; Procario, Megan C.2 ; Weinberg, Jason B.1,2
- Source:
Virology. May2014, Vol. 456-457, p259-267. 9p.- Subject Terms:
- Source:
- Additional Information
- Abstract: Abstract: 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. [Copyright &y& Elsevier]
- Abstract: Copyright of Virology is the property of Academic Press Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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