ArticlePloS one2013
TNF-Α may mediate inflammasome activation in the absence of bacterial infection in more than one way.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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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Who cites it
31 citing papers in PubMed, 65 citations in OpenAlex.
- Remodeling the Immune Landscape: How Obesity-Induced SASPs Create a Pro-Tumorigenic Niche.Current obesity reports · 2026Review
- The NOX2-ROS-NLRP3 inflammasome axis in traumatic brain injury.Journal of neuroinflammation · 2025Article
- Animal and cellular models of atrial fibrillation: a review.Frontiers in cardiovascular medicine · 2025Review
- Review
- Evaluation of the innate immune response of caprine neutrophils against Mycobacterium avium subspecies paratuberculosis in vitro.Veterinary research · 2023Article
- Chronic cerebral aspects of long COVID, post-stroke syndromes and similar states share their pathogenesis and perispinal etanercept treatment logic.Pharmacology research & perspectives · 2022Review
- A Pro-Inflammatory Signature Constitutively Activated in Monogenic Autoinflammatory Diseases.International journal of molecular sciences · 2022Article
- Renal plasticity revealed through reversal of polycystic kidney disease in mice.Nature genetics · 2021Article
- Blood-brain barrier opening by intracarotid artery hyperosmolar mannitol induces sterile inflammatory and innate immune responses.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Effect ofThe journal of venomous animals and toxins including tropical diseases · 2020Article
- Essential role of Salmonella Enteritidis DNA adenine methylase in modulating inflammasome activation.BMC microbiology · 2020Article
- UV-B-Induced Inflammasome Activation Can Be Prevented by Cis-Urocanic Acid in Human Corneal Epithelial Cells.Investigative ophthalmology & visual science · 2020Article
- Inflammasome Activation in Human Macrophages Induced by a LDL (-) Mimetic Peptide.Inflammation · 2020Article
- Acylated Ghrelin as a Multi-Targeted Therapy for Alzheimer's and Parkinson's Disease.Frontiers in neuroscience · 2020Review
- Article
- CRP-Induced NLRP3 Inflammasome Activation Increases LDL Transcytosis Across Endothelial Cells.Frontiers in pharmacology · 2019Article
- TNF, but not hyperinsulinemia or hyperglycemia, is a key driver of obesity-induced monocytosis revealing that inflammatory monocytes correlate with insulin in obese male mice.Physiological reports · 2018Article
- Caspase-1 inhibition prevents glial inflammasome activation and pyroptosis in models of multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Inhibition of the NLRP3-inflammasome as a potential approach for neuroprotection after stroke.Scientific reports · 2018Article
- A high concentration of DMSO activates caspase-1 by increasing the cell membrane permeability of potassium.Cytotechnology · 2018Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Members of the mammalian nucleotide binding domain, leucine-rich repeat (LRR)-containing receptor family of proteins are key modulators of innate immunity regulating inflammation. To date, microbial pathogen-associated molecules and toxins have been identified as key triggers of activation of inflammasomes. However, recently, environmental, and neurodegenerative stimuli have been identified that lead to IL-1β release by means of inflammasomes. IL-1β plays a crucial role during brain inflammation, and caspase-1 appears to be a key modulator of IL-1β bioactivity and the consequent transcriptional regulation of gene expression within the brain during inflammation. We show here that exposure of a human neuroblastoma cell line (SK-N-MC cells) to TNF-α promotes ROS-mediated caspase-1 activation and IL-1β secretion. The involvement of NF-κB in the regulation of IL-1β synthesis is investigated through specific inhibition of this transcription factor. The effect of TNF-α was abolished in the presence of ROS inhibitors as NAC, or DPI. Remarkably, SK-N-MC cells do not respond to ATP stimulation in spite of P2X7R expression. These results provide a mechanism by which danger signals and particulate matter mediate inflammation via the inflammasome in the absence of microbial 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.