ArticleEMBO molecular medicine2014
Activation of IL-27 signalling promotes development of postinfluenza pneumococcal pneumonia.
Article in EMBO molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 82 citations in OpenAlex.
- Type I interferon signaling in hematopoietic cells impairs neutrophil antibacterial function in the middle ear during viral co-infection.Cell reports. Medicine · 2026Article
- Current insights into bacterial secondary infection following influenza A virus infection.Frontiers in microbiology · 2026Review
- Type I Interferon Targets Alveolar Macrophages to Promote Bacterial Pneumonia after Viral Infection.American journal of respiratory cell and molecular biology · 2025Article
- Early application of extracorporeal membrane oxygenation in influenza B virus-related fulminant pneumonia complicated with methicillin-sensitiveFrontiers in medicine · 2025Article
- Post-influenza bacterial infection: mechanisms of pathogenesis and advances in therapeutic strategies.Frontiers in microbiology · 2025Review
- High-sensitive sensory neurons exacerbate rosacea-like dermatitis in mice by activating γδ T cells directly.Nature communications · 2024Article
- IL-27 disturbs lipid metabolism and restrains mitochondrial activity to inhibit γδ T17 cell-mediated skin inflammation.Cell death & disease · 2024Article
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- Human monoclonal antibodies protect against viral-mediated pneumococcal superinfection.Frontiers in immunology · 2024Article
- Synthetic BSA-conjugated disaccharide related to theFrontiers in immunology · 2024Article
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- IL-27 Signaling Promotes Th1 Response by Downregulating IL-10 Production in DCs during Chlamydial Respiratory Infection.Microorganisms · 2023Article
- Immune predisposition drives susceptibility to pneumococcal pneumonia after mild influenza A virus infection in mice.Frontiers in immunology · 2023Article
- Type I IFN Signaling Is Essential for Preventing IFN-γ Hyperproduction and Subsequent Deterioration of Antibacterial Immunity during Postinfluenza Pneumococcal Infection.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Impact of Type I Interferons on Susceptibility to Bacterial Pathogens.Trends in microbiology · 2021Review
- Review
- Virus-Induced Changes of the Respiratory Tract Environment Promote Secondary Infections WithFrontiers in cellular and infection microbiology · 2021Review
- Host Immune Responses toFrontiers in microbiology · 2021Review
- Role of γδ T cells in controlling viral infections with a focus on influenza virus: implications for designing novel therapeutic approaches.Virology journal · 2020Review
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Postinfluenza pneumococcal pneumonia is a common cause of death in humans. However, the role of IL-27 in the pathogenesis of secondary pneumococcal pneumonia after influenza is unknown. We now report that influenza infection induced pulmonary IL-27 production in a type I IFN-α/β receptor (IFNAR) signalling-dependent manner, which sensitized mice to secondary pneumococcal infection downstream of IFNAR pathway. Mice deficient in IL-27 receptor were resistant to secondary pneumococcal infection and generated more IL-17A-producing γδ T cells but not αβ T cells, thereby leading to enhanced neutrophil response during the early phase of host defence. IL-27 treatment could suppress the development of IL-17A-producing γδ T cells activated by Streptococcus pneumoniae and dendritic cells. This suppressive activity of IL-27 on γδ T cells was dependent on transcription factor STAT1. Finally, neutralization of IL-27 or administration of IL-17A restored the role of γδ T cells in combating secondary pneumococcal infection. Our study defines what we believe to be a novel role of IL-27 in impairing host innate immunity against pneumococcal infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.