ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Influenza A exacerbates Staphylococcus aureus pneumonia by attenuating IL-1β production in mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.
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Who cites it
94 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.
- Immunopathological Changes in SARS-CoV-2 Critical and Non-critical Pneumonia Patients: A Systematic Review to Determine the Cause of Co-infection.Frontiers in public health · 2020Pooled it
- Diabetes Mellitus with Influenza Virus and Subsequent Bacterial Infection: Triple Pathological Interactions and Challenges.International journal of molecular sciences · 2026Review
- Hypoxia-inducible factor-1α exacerbates immune injury induced by influenza A virus and Streptococcus pneumoniae coinfection.BMC infectious diseases · 2025Article
- Preceding influenza infection impacts neutrophil response to Aspergillus fumigatus and Staphylococcus aureus.ImmunoHorizons · 2025Article
- Influenza virus and Staphylococcus aureus super-infection disrupts spatially coordinated cellular immunity in the mouse lung.Communications biology · 2025Article
- Vital Role of PINK1/Parkin-Mediated Mitophagy of Pulmonary Epithelial Cells in Severe Pneumonia Induced by IAV and SecondaryInternational journal of molecular sciences · 2025Article
- Harnessing Epigenetics: Innovative Approaches in Diagnosing and Combating Viral Acute Respiratory Infections.Pathogens (Basel, Switzerland) · 2025Review
- Therapeutic JAK inhibition does not impact lung injury during viral or bacterial pneumonia in male mice.Physiological reports · 2025Article
- CD209d/e promotes inflammation and lung injury during influenza virus infection.ImmunoHorizons · 2025Article
- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
- Restoration of Type 17 immune signaling is not sufficient for protection during influenza-associated pulmonary aspergillosis.Frontiers in immunology · 2025Article
- Treatment with lipoxin AInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Restoration of Type 17 immune signaling is not sufficient for protection during influenza-associated pulmonary aspergillosis.bioRxiv : the preprint server for biology · 2024Article
- Treatment with lipoxin A 4 improves influenza A infection outcome through macrophage reprogramming, anti-inflammatory and pro-resolutive responses.Research square · 2024Article
- Activation of the RIG-I/MAVS Signaling Pathway during Human Adenovirus Type 3 Infection Impairs the Pro-Inflammatory Response Induced by Secondary Infection withInternational journal of molecular sciences · 2024Article
- cGLRs Join Their Cousins of Pattern Recognition Receptor Family to Regulate Immune Homeostasis.International journal of molecular sciences · 2024Review
- The Dual Roles of Activating Transcription Factor 3 (ATF3) in Inflammation, Apoptosis, Ferroptosis, and Pathogen Infection Responses.International journal of molecular sciences · 2024Review
- Streptococcus pyogenes Pneumonia: A Rare and Severe Presentation in a Patient With Asthma.Cureus · 2023Article
- Article
- Influenza A-induced cystic fibrosis transmembrane conductance regulator dysfunction increases susceptibility to Streptococcus pneumoniae.JCI insight · 2023Article
34 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Pneumonia is a leading cause of death worldwide. Staphylococcal aureus can be a cause of severe pneumonia alone or a common pathogen in secondary pneumonia following influenza. Recently, we reported that preceding influenza attenuated the Type 17 pathway, increasing the lung's susceptibility to secondary infection. IL-1β is known to regulate host defense, including playing a role in Th17 polarization. We examined whether IL-1β signaling is required for S. aureus host defense and whether influenza infection impacted S. aureus-induced IL-1β production and subsequent Type 17 pathway activation. Mice were challenged with S. aureus (USA 300), with or without preceding Influenza A/PR/8/34 H1N1 infection. IL-1R1(-/-) mice had significantly higher S. aureus burden, increased mortality, and decreased Type 17 pathway activation following S. aureus challenge. Coinfected mice had significantly decreased IL-1β production versus S. aureus infection alone at early time points following bacterial challenge. Preceding influenza did not attenuate S. aureus-induced inflammasome activation, but there was early suppression of NF-κB activation, suggesting an inhibition of NF-κB-dependent transcription of pro-IL-1β. Furthermore, overexpression of IL-1β in influenza and S. aureus-coinfected mice rescued the induction of IL-17 and IL-22 by S. aureus and improved bacterial clearance. Finally, exogenous IL-1β did not significantly rescue S. aureus host defense during coinfection in IL-17RA(-/-) mice or in mice in which IL-17 and IL-22 activity were blocked. These data reveal a novel mechanism by which Influenza A inhibits S. aureus-induced IL-1β production, resulting in attenuation of Type 17 immunity and increased susceptibility to bacterial 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.