ArticleNature communications2014
TRPA1 channels mediate acute neurogenic inflammation and pain produced by bacterial endotoxins.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 268 papers, 2 of them syntheses that pooled it.
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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.
The trial behind it
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
268 citing papers in PubMed, 2 syntheses or guidelines pooled it, 466 citations in OpenAlex.
- Neural biomarkers in pulpitis and their associations with inflammation and pain perception: a systematic review and meta-analysis.BMC oral health · 2026Pooled it
- Enterochromaffin Cells: Sentinels to Gut Microbiota in Hyperalgesia?Frontiers in cellular and infection microbiology · 2021Pooled it
- RAGE mediates LPS-induced inflammatory pain in human skin - a double-blind, randomised, placebo-controlled full crossover study.Nature communications · 2026Trial
- Oral and Intestinal Bacterial Substances Associated with Disease Activities in Patients with Rheumatoid Arthritis: A Cross-Sectional Clinical Study.Journal of immunology research · 2022Trial
- A Human TRPA1-Specific Pain Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Trial
- Neuro-immune interactions in tumors, immune-related disorders, and infections.Signal transduction and targeted therapy · 2026Review
- Two pore domain THIK2 potassium channels regulate acute and chronic pain signaling.Pain reports · 2026Article
- A single-point mutation in TRPA1 drives heat resilience in oviparous embryos.Science advances · 2026Article
- Neurogenic Rosacea and Facial Dysesthesia: Neurovascular-Immune Mechanisms and Translational Therapeutic Perspectives.Medicina (Kaunas, Lithuania) · 2026Review
- The miR-183/96/182 Cluster Regulates Trigeminal Ganglion Sensory Neurons' Response toPathogens (Basel, Switzerland) · 2026Article
- Bidirectional crosstalk between TRP channels and Toll-like receptors in inflammation and host defense.Journal of neuroinflammation · 2026Review
- Vagal neuropathies: An underrecognized potential driver of physical, mental, and immune symptoms.Brain, behavior, & immunity - health · 2026Review
- TRPA1 Integrates Nociceptive and Immune Signaling inInternational journal of molecular sciences · 2026Article
- Identification of bacterial signals that modulate enteric sensory neurons to influence behavior in C. elegans.Current biology : CB · 2026Article
- Review
- Validation of TRPA1 and TRPV1 Antibodies for Expression Detection in Mammalian Cells and Tissues.Journal of neurochemistry · 2026Article
- The miR-183/96/182 Cluster Regulates Trigeminal Ganglion Sensory Neurons' Response tobioRxiv : the preprint server for biology · 2026Article
- Reduced Neuroinflammation and Pain with a Functional Sourdough Bread Enriched with Legumes and Ancient Cereals in a Mouse Model of LPS-Induced Inflammation.International journal of molecular sciences · 2026Article
- Neural Circuits between Nodose Ganglion and Pulmonary Neuroendocrine Cells Regulate Lung Inflammatory Responses.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- LPS-induced structural reorganization and polymerization drive noncanonical inflammasome activation.Science advances · 2026Article
208 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
20 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gram-negative bacterial infections are accompanied by inflammation and somatic or visceral pain. These symptoms are generally attributed to sensitization of nociceptors by inflammatory mediators released by immune cells. Nociceptor sensitization during inflammation occurs through activation of the Toll-like receptor 4 (TLR4) signalling pathway by lipopolysaccharide (LPS), a toxic by-product of bacterial lysis. Here we show that LPS exerts fast, membrane delimited, excitatory actions via TRPA1, a transient receptor potential cation channel that is critical for transducing environmental irritant stimuli into nociceptor activity. Moreover, we find that pain and acute vascular reactions, including neurogenic inflammation (CGRP release) caused by LPS are primarily dependent on TRPA1 channel activation in nociceptive sensory neurons, and develop independently of TLR4 activation. The identification of TRPA1 as a molecular determinant of direct LPS effects on nociceptors offers new insights into the pathogenesis of pain and neurovascular responses during bacterial infections and opens novel avenues for their treatment.
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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.