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© Research
Publication : Journal of virology

Interleukin-22 reduces lung inflammation during influenza A virus infection and protects against secondary bacterial infection

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Journal of virology - 17 Apr 2013

Ivanov S, Renneson J, Fontaine J, Barthelemy A, Paget C, Fernandez EM, Blanc F, De Trez C, Van Maele L, Dumoutier L, Huerre MR, Eberl G, Si-Tahar M, Gosset P, Renauld JC, Sirard JC, Faveeuw C, Trottein F

Link to Pubmed [PMID] – 23596287

J. Virol. 2013 Jun;87(12):6911-24

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-γt (RORγt)-positive αβ and γδ 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.

http://www.ncbi.nlm.nih.gov/pubmed/23596287