tetano
Editor, Senior Moderator
J Virol. 2013 Apr 17. [Epub ahead of print]
Interleukin-22 reduces lung inflammation during influenza A virus infection and protects against secondary bacterial infection.
Ivanov S, Renneson J, Fontaine J, Barthelemy A, Paget C, Macho Fernandez E, 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.
Source
Institut Pasteur de Lille, Centre d'Infection et d'Immunit? de Lille, F-59019 Lille, France.
Abstract
Interleukin (IL)-22 has redundant, protective or pathogenic functions during auto-immune, inflammatory and infectious diseases. Here, we addressed the potential role of IL-22 in host defence 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 RORγt-positive αβ and γδ T cells, as well as innate lymphoid cells, expressed enhanced Il22 transcripts as early as two days post-infection. 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 an enhanced lung injury 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.
PMID:
23596287
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23596287
Interleukin-22 reduces lung inflammation during influenza A virus infection and protects against secondary bacterial infection.
Ivanov S, Renneson J, Fontaine J, Barthelemy A, Paget C, Macho Fernandez E, 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.
Source
Institut Pasteur de Lille, Centre d'Infection et d'Immunit? de Lille, F-59019 Lille, France.
Abstract
Interleukin (IL)-22 has redundant, protective or pathogenic functions during auto-immune, inflammatory and infectious diseases. Here, we addressed the potential role of IL-22 in host defence 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 RORγt-positive αβ and γδ T cells, as well as innate lymphoid cells, expressed enhanced Il22 transcripts as early as two days post-infection. 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 an enhanced lung injury 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.
PMID:
23596287
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23596287