期刊
JOURNAL OF VIROLOGY
卷 87, 期 12, 页码 6911-6924出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.02943-12
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资金
- Institut National de la Sante et de la Recherche Medicale
- CNRS
- University of Lille Nord de France
- Pasteur Institute of Lille
- l'Agence Nationale de la Recherche (ANR) [ANR-08-MIEN-021-01]
- Ministere de l'Education Nationale de la Recherche et Technique
- Conseil Regional Nord Pas de Calais/Inserm
- ANR [ANR-08-MIEN-021-01]
- Hopital Saint Vincent (Lille)
- FNRS
- Inserm
Interleukin-22 (IL-22) has redundant, protective, or pathogenic functions during autoimmune, inflammatory, and infectious diseases. Here, we addressed the potential role of IL-22 in host defense and pathogenesis during lethal and sublethal respiratory H3N2 influenza A virus (IAV) infection. We show that IL-22, as well as factors associated with its production, are expressed in the lung tissue during the early phases of IAV infection. Our data indicate that retinoic acid receptor-related orphan receptor-gamma t (ROR gamma t)-positive alpha beta and gamma delta T cells, as well as innate lymphoid cells, expressed enhanced Il22 transcripts as early as 2 days postinfection. During lethal or sublethal IAV infections, endogenous IL-22 played no role in the control of IAV replication and in the development of the IAV-specific CD8(+) T cell response. During lethal infection, where wild-type (WT) mice succumbed to severe pneumonia, the lack of IL-22 did not accelerate or delay IAV-associated pathogenesis and animal death. In stark contrast, during sublethal IAV infection, IL-22-deficient animals had enhanced lung injuries and showed a lower airway epithelial integrity relative to WT littermates. Of importance, the protective effect of endogenous IL-22 in pulmonary damages was associated with a more controlled secondary bacterial infection. Indeed, after challenge with Streptococcus pneumoniae, IAV-experienced Il22(-/-) animals were more susceptible than WT controls in terms of survival rate and bacterial burden in the lungs. Together, IL-22 plays no major role during lethal influenza but is beneficial during sublethal H3N2 IAV infection, where it limits lung inflammation and subsequent bacterial superinfections.
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