ArticleEMBO reports2015
TRAIL+ monocytes and monocyte-related cells cause lung damage and thereby increase susceptibility to influenza-Streptococcus pneumoniae coinfection.
Article in EMBO reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
68 citing papers in PubMed, 97 citations in OpenAlex.
- Type I IFN coordinates resistance and tolerance against Zika virus disease by inducing NK cell recruitment and limiting neutrophil-driven neuropathology in the brain.Brain, behavior, & immunity - health · 2026Article
- TNF superfamily member 14 drives post-influenza depletion of alveolar macrophages, enabling secondary pneumococcal pneumonia.The Journal of clinical investigation · 2026Article
- Hypoxia-inducible factor-1α exacerbates immune injury induced by influenza A virus and Streptococcus pneumoniae coinfection.BMC infectious diseases · 2025Article
- Loss of pulmonary tissue protection and neutrophil microbicidal defects promote severeInfection and immunity · 2025Article
- Maladaptive trained immunity in viral infections.The Journal of clinical investigation · 2025Review
- Type I Interferon Targets Alveolar Macrophages to Promote Bacterial Pneumonia after Viral Infection.American journal of respiratory cell and molecular biology · 2025Article
- Post-influenza bacterial infection: mechanisms of pathogenesis and advances in therapeutic strategies.Frontiers in microbiology · 2025Review
- Association of circulating cytokine levels and tissue-infiltrating myeloid cells with achalasia: results from Mendelian randomization and validation through clinical characteristics and single-cell RNA sequencing.Journal of gastroenterology · 2024Article
- Type 1 interferons promote Staphylococcus aureus nasal colonization by inducing phagocyte apoptosis.Cell death discovery · 2024Article
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- Immunological Signatures in Blood and Urine in 80 Individuals Hospitalized during the Initial Phase of COVID-19 Pandemic with Quantified Nicotine Exposure.International journal of molecular sciences · 2024Article
- Neutrophils in Physiology and Pathology.Annual review of pathology · 2024Review
- Human monoclonal antibodies protect against viral-mediated pneumococcal superinfection.Frontiers in immunology · 2024Article
- Mathematical Modeling of the Lethal Synergism of Coinfecting Pathogens in Respiratory Viral Infections: A Review.Microorganisms · 2023Review
- Article
- Microbial and Immune Regulation of the Gut-Lung Axis during Viral-Bacterial Coinfection.Journal of bacteriology · 2023Review
- Pathogenesis of pneumonia and acute lung injury.Clinical science (London, England : 1979) · 2022Review
- IL-6 Prevents Lung Macrophage Death and Lung Inflammation Injury by Inhibiting GSDME- and GSDMD-Mediated Pyroptosis during Pneumococcal Pneumosepsis.Microbiology spectrum · 2022Article
- Article
- Pathogenesis of Respiratory Viral and Fungal Coinfections.Clinical microbiology reviews · 2022Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Streptococcus pneumoniae coinfection is a major cause of influenza-associated mortality; however, the mechanisms underlying pathogenesis or protection remain unclear. Using a clinically relevant mouse model, we identify immune-mediated damage early during coinfection as a new mechanism causing susceptibility. Coinfected CCR2(-/-) mice lacking monocytes and monocyte-derived cells control bacterial invasion better, show reduced epithelial damage and are overall more resistant than wild-type controls. In influenza-infected wild-type lungs, monocytes and monocyte-derived cells are the major cell populations expressing the apoptosis-inducing ligand TRAIL. Accordingly, anti-TRAIL treatment reduces bacterial load and protects against coinfection if administered during viral infection, but not following bacterial exposure. Post-influenza bacterial outgrowth induces a strong proinflammatory cytokine response and massive inflammatory cell infiltrate. Depletion of neutrophils or blockade of TNF-α facilitate bacterial outgrowth, leading to increased mortality, demonstrating that these factors aid bacterial control. We conclude that inflammatory monocytes recruited early, during the viral phase of coinfection, induce TRAIL-mediated lung damage, which facilitates bacterial invasion, while TNF-α and neutrophil responses help control subsequent bacterial outgrowth. We thus identify novel determinants of protection versus pathology in influenza-Streptococcus pneumoniae coinfection.
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What OpenQuestion holds
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.