ArticleJournal of neurogastroenterology and motility2010
Viewpoints on Acid-induced inflammatory mediators in esophageal mucosa.
Article in Journal of neurogastroenterology and motility, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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
17 citing papers in PubMed, 27 citations in OpenAlex.
- Impact of PAR2 on Tight Junctions and Esophageal Mucosal Inflammation in Rats with Gastroesophageal Reflux Disease.Neurogastroenterology and motility · 2026Article
- Neuro-immune-epithelial pathways involving substance P may contribute to mucosal pathology in gastro-oesophageal reflux disease.Frontiers in immunology · 2026Article
- Microbiota profiling in esophageal diseases: Novel insights into molecular staining and clinical outcomes.Computational and structural biotechnology journal · 2024Review
- Mucosal neuroimmune mechanisms in gastro-oesophageal reflux disease (GORD) pathogenesis.Journal of gastroenterology · 2024Review
- Protective Effects of Inflammation of Curcumae Longae Rhizoma 30% EtOH Extract on Acute Reflux Esophagitis Rats.BioMed research international · 2021Article
- Is the Lower Esophageal Sphincter Tone Related to a Gas?Cellular and molecular gastroenterology and hepatology · 2018Article
- Exploration of the Esophageal Mucosal Barrier in Non-Erosive Reflux Disease.International journal of molecular sciences · 2017Article
- Upregulation of the transient receptor potential vanilloid 1 in colonic epithelium of patients with active inflammatory bowel disease.International journal of clinical and experimental pathology · 2017Article
- Mechanisms of the adenosine A2A receptor-induced sensitization of esophageal C fibers.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- A stepwise protocol for the treatment of refractory gastroesophageal reflux-induced chronic cough.Journal of thoracic disease · 2016Article
- Does Measurement of Esophagogastric Junction Distensibility by EndoFLIP Predict Therapy- responsiveness to Endoluminal Fundoplication in Patients With Gastroesophageal Reflux Disease?Journal of neurogastroenterology and motility · 2015Article
- Long-term maintenance effect of radiofrequency energy delivery for refractory GERD: a decade later.Surgical endoscopy · 2014Article
- NERD: an umbrella term including heterogeneous subpopulations.Nature reviews. Gastroenterology & hepatology · 2013Review
- Esophageal intraluminal baseline impedance is associated with severity of acid reflux and epithelial structural abnormalities in patients with gastroesophageal reflux disease.Journal of gastroenterology · 2013Article
- Distinction between patients with non-erosive reflux disease and functional heartburn.Annals of gastroenterology · 2013Review
- Gastroesophageal reflux disease in children and adolescents: when and how to treat.Paediatric drugs · 2012Review
- Preferential activation of the vagal nodose nociceptive subtype by TRPA1 agonists in the guinea pig esophagus.Neurogastroenterology and motility · 2011Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
We have focused on understanding the onset of gastroesophageal reflux disease by examining the mucosal response to the presence of acid in the esophageal lumen. Upon exposure to HCl, inflammation of the esophagus begins with activation of the transient receptor potential channel vanilloid subfamily member-1 (TRPV1) in the mucosa, and production of IL-8, substance P (SP), calcitonin gene related peptide (CGRP) and platelet activating factor (PAF). Production of SP and CGRP, but not PAF, is abolished by the neural blocker tetrodotoxin suggesting that SP and CGRP are neurally released and that PAF arises from non neural pathways. Epithelial cells contain TRPV1 receptor mRNA and protein and respond to HCl and to the TRPV1 agonist capsaicin with production of PAF. PAF, SP and IL-8 act as chemokines, inducing migration of peripheral blood leukocytes. PAF and SP activate peripheral blood leukocytes inducing the production of H(2)O(2). In circular muscle, PAF causes production of IL-6, and IL-6 causes production of additional H(2)O(2), through activation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidases. Among these, NADPH oxidase 5 cDNA is significantly up-regulated by exposure to PAF; H(2)O(2) content of esophageal and lower esophageal sphincter circular muscle is elevated in human esophagitis, causing dysfunction of esophageal circular muscle contraction and reduction in esophageal sphincter tone. Thus esophageal keratinocytes, that constitute the first barrier to the refluxate, may also serve as the initiating cell type in esophageal inflammation, secreting inflammatory mediators and pro-inflammatory cytokines and affecting leukocyte recruitment and activity.
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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.