ArticleInfection and immunity2013
Shedding of tumor necrosis factor receptor 1 induced by protein A decreases tumor necrosis factor alpha availability and inflammation during systemic Staphylococcus aureus infection.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 57 citations in OpenAlex.
- scImmuneCo: a compendium of cell-type-specific functional modules for decoding immune responses from single-cell RNA-seq data.Briefings in bioinformatics · 2026Article
- Integrative network pharmacology and experimental validation of rubus ulmifolius leaf extract in a rat model of MRSA-infected wounds.Inflammopharmacology · 2026Article
- E3 ubiquitin ligase SKP2 limits autophagosome formation duringFrontiers in cellular and infection microbiology · 2026Article
- Preceding influenza infection impacts neutrophil response to Aspergillus fumigatus and Staphylococcus aureus.ImmunoHorizons · 2025Article
- Hybrid Receptor-Mediated Molecular Delineations in TNF-α and IGF-1-Induced Costimulatory Effects.International journal of molecular sciences · 2025Article
- Role of Tumor Necrosis Factor in Tuberculosis.Biomolecules · 2025Review
- Infections in Patients with Atopic Dermatitis and the Influence of Treatment.American journal of clinical dermatology · 2025Review
- Neutrophil-intrinsic TNF receptor signaling orchestrates host defense againstScience advances · 2023Article
- Neutralization of Staphylococcus aureus Protein A Prevents Exacerbated Osteoclast Activity and Bone Loss during Osteomyelitis.Antimicrobial agents and chemotherapy · 2023Article
- Nuclease activity and protein A release ofFrontiers in immunology · 2023Article
- In Silico Genome-Scale Analysis of Molecular Mechanisms Contributing to the Development of a Persistent Infection with Methicillin-ResistantInternational journal of molecular sciences · 2022Article
- Cutaneous dysbiosis may amplify barrier dysfunction in patients with atopic dermatitis.Frontiers in microbiology · 2022Article
- Immune-Enhancing Effects of Co-treatment WithFrontiers in nutrition · 2022Article
- Immune control of Mycobacterium tuberculosis is dependent on both soluble TNFRp55 and soluble TNFRp75.Immunology · 2021Article
- Severe COVID-19 Patients Show an Increase in Soluble TNFR1 and ADAM17, with a Relationship to Mortality.International journal of molecular sciences · 2021Article
- Pathophysiology and management of critical illness polyneuropathy and myopathy.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- The STAPH Score: A Predictor ofOpen forum infectious diseases · 2021Article
- Leucine-Rich α-2-Glycoprotein 1 Suppresses Endothelial Cell Activation Through ADAM10-Mediated Shedding of TNF-α Receptor.Frontiers in cell and developmental biology · 2021Article
- TNFR1, TNFR2, neutrophil gelatinase-associated lipocalin and heparin binding protein in identifying sepsis and predicting outcome in an intensive care cohort.Scientific reports · 2020Observational
- Cellular signalling pathways mediating the pathogenesis of chronic inflammatory respiratory diseases: an update.Inflammopharmacology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Staphylococcus aureus infections are an important public health concern due to their increasing incidence and high rates of mortality. The success of S. aureus as a pathogen is highly related to its enormous capacity to evade the host immune response. The critical role of tumor necrosis factor alpha (TNF-α) in the initial host defense against systemic staphylococcal infection has been demonstrated in experimental models and may partially explain the lack of significant benefits observed in clinical trials attempting to neutralize this cytokine in septic patients. S. aureus protein A plays a key role in regulating inflammation through its ability to bind and signal through the TNF-α receptor 1 (TNFR1). In this study, we demonstrate that S. aureus, via protein A-mediated signaling, induces early shedding of TNFR1, which precedes the secretion of TNF-α in vitro and in vivo. The results obtained using a protein A-deficient mutant and tnfr1(-/-) mice strongly suggest that the increased levels of soluble TNFR1 present during experimental S. aureus infection may neutralize circulating TNF-α and impair the host inflammatory response. Early shedding of TNFR1 induced by protein A may constitute a novel mechanism by which S. aureus subverts the host immune response.
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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.