Interleukin-22 reduces lung inflammation during influenza A virus infection and protects against secondary bacterial infection. - Archive ouverte HAL Access content directly
Journal Articles Journal of Virology Year : 2013

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

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Fany Blanc
Gérard Eberl
Mustapha Si-Tahar

Abstract

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.

Dates and versions

inserm-00926618 , version 1 (09-01-2014)

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Stoyan Ivanov, Joelle Renneson, Josette Fontaine, Adeline Barthelemy, Christophe Paget, et al.. Interleukin-22 reduces lung inflammation during influenza A virus infection and protects against secondary bacterial infection.. Journal of Virology, 2013, 87 (12), pp.6911-24. ⟨10.1128/JVI.02943-12⟩. ⟨inserm-00926618⟩
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