title: IL-17 contributes to neutrophil recruitment but not to control of viral replication during acute mouse adenovirus type 1 respiratory infection.
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.
authors.affiliation: Department of Microbiology and Immunology, University of Michigan, 5641 Medical Science Building II, 1150 West Medical Center Drive, Ann Arbor, MI 48109, USA. Electronic address: mkmccar@umich.edu.
authors.forename: Mary K
authors.initials: MK
authors.lastname: McCarthy
authors.affiliation: Department of Microbiology and Immunology, University of Michigan, 5641 Medical Science Building II, 1150 West Medical Center Drive, Ann Arbor, MI 48109, USA. Electronic address: lingqiao.zhu@gmail.com.
authors.forename: Lingqiao
authors.initials: L
authors.lastname: Zhu
authors.affiliation: Department of Pediatrics and Communicable Diseases, University of Michigan, 7510A Medical Science Research Building I, 1150 West Medical Center Drive, Ann Arbor, MI 48109, USA. Electronic address: mcprocar@umich.edu.
authors.forename: Megan C
authors.initials: MC
authors.lastname: Procario
authors.affiliation: Department of Microbiology and Immunology, University of Michigan, 5641 Medical Science Building II, 1150 West Medical Center Drive, Ann Arbor, MI 48109, USA; Department of Pediatrics and Communicable Diseases, University of Michigan, 7510A Medical Science Research Building I, 1150 West Medical Center Drive, Ann Arbor, MI 48109, USA. Electronic address: jbwein@umich.edu.
authors.forename: Jason B
authors.initials: JB
authors.lastname: Weinberg
mesh_terms: D000256:Adenoviridae / Q000276:immunology* / Q000502:physiology; D000257:Adenoviridae Infections / Q000276:immunology*; D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D004195:Disease Models, Animal; D054884:Host-Pathogen Interactions; D006801:Humans; D020381:Interleukin-17 / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D020556:Neutrophil Infiltration; D012141:Respiratory Tract Infections / Q000276:immunology*; D014779:Virus Replication
chemical_list: D020381:Interleukin-17
keywords: Adenovirus; IL-17; Rspiratory infection; Th17