ArticleMucosal immunology2014
Secretion of IL-16 through TNFR1 and calpain-caspase signaling contributes to MRSA pneumonia.
Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Single-cell hdWGCNA identifies checkpoint inhibitor pneumonitis-linked CD4 + T-cell subsets driving immunotherapy response and prognosis in lung cancer.Journal of cancer research and clinical oncology · 2026Article
- NLRP3 promotes inflammatory signaling and IL-1β cleavage in acute lung injury caused by cell wall extract of Lactobacillus casei.Communications biology · 2025Article
- Role of interleukin-16 in human diseases: a novel potential therapeutic target.Frontiers in immunology · 2025Review
- Article
- Hyperalgesic Effect Evoked by il-16 and its Participation in Inflammatory Hypernociception in Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Article
- Exploring secretory proteome and cytokine kinetic of human peripheral blood mononuclear cells exposed to methicillin-resistantFrontiers in immunology · 2024Article
- Review
- Anti-Interleukin-16-Neutralizing Antibody Attenuates Cardiac Inflammation and Protects against Cardiac Injury in Doxorubicin-Treated Mice.Mediators of inflammation · 2021Article
- Mesenchymal stem cells significantly improved treatment effects of Linezolid on severe pneumonia in a rabbit model.Bioscience reports · 2019Article
- IL-16/miR-125a axis controls neutrophil recruitment in pristane-induced lung inflammation.JCI insight · 2018Article
- Dual roles of calpain in facilitating Coxsackievirus B3 replication and prompting inflammation in acute myocarditis.International journal of cardiology · 2016Article
- Macrophage-epithelial interactions in pulmonary alveoli.Seminars in immunopathology · 2016Review
- Innate Immune Signaling Activated by MDR Bacteria in the Airway.Physiological reviews · 2016Review
- CD4+ T cells promote the pathogenesis of Staphylococcus aureus pneumonia.The Journal of infectious diseases · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Staphylococcus aureus is a major cause of severe pneumonia. Multiple mechanisms of proinflammatory signaling are activated to recruit immune cells into the airway in response to S. aureus. We found that interleukin-16 (IL-16), a T cell cytokine that binds CD4, is potently activated by S. aureus, specifically by protein A (SpA), and to a much greater extent than by Gram-negative pathogens or lipopolysaccharide. IL-16 production involved multiple signals including ligation of tumor necrosis factor receptor (TNFR) family members or epidermal growth factor receptor, both receptors for SpA and generation of Ca(2+) fluxes to activate calpains and caspase-3. Although human airway epithelial cells, vascular endothelial cells, THP-1 and Jurkat T cells released IL-16 in response to S. aureus in vitro, in a murine model of pneumonia, CD4(+) cells were the major source of IL-16 suggesting the involvement of an autocrine signaling pathway. The production of IL-16 contributed to lung damage as neutralization of IL-16 enhanced S. aureus clearance and resulted in diminished lung pathology in S. aureus pneumonia. Our results suggest that the ability of S. aureus to activate TNFR1 and Ca(2+)/calpain signaling contribute to T cell activation and excessive inflammation in the setting of acute pneumonia.
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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.