ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2010
HCl-induced inflammatory mediators in esophageal mucosa increase migration and production of H2O2 by peripheral blood leukocytes.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- The effect of SP/NK1R on expression and activity of glutaredoxin and thioredoxin proteins in prostate cancer cells.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Trends in gastroesophageal reflux disease research: A bibliometric and visualized study.Frontiers in medicine · 2022Article
- Pathogenic role of the SP/ NK1R system in GBM cells through inhibiting the thioredoxin system.Iranian journal of basic medical sciences · 2021Article
- Pathophysiology and treatment options for gastroesophageal reflux disease: looking beyond acid.Annals of the New York Academy of Sciences · 2021Review
- Lactobacillus reuteri DSM 17938 Protects against Gastric Damage Induced by Ethanol Administration in Mice: Role of TRPV1/Substance P Axis.Nutrients · 2019Article
- Nonalcoholic fatty liver disease increases risk for gastroesophageal reflux symptoms.Digestive diseases and sciences · 2014Article
- pH of drinking water influences the composition of gut microbiome and type 1 diabetes incidence.Diabetes · 2014Article
- Gastroesophageal reflux disease: Update on inflammation and symptom perception.World journal of gastroenterology · 2013Review
- Stromal cells participate in the murine esophageal mucosal injury response.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- Platelet-activating factor and distinct chemokines are elevated in mucosal biopsies of erosive compared with non-erosive reflux disease patients and controls.Neurogastroenterology and motility · 2012Article
- HCl-induced and ATP-dependent upregulation of TRPV1 receptor expression and cytokine production by human esophageal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- ATP: a mediator for HCl-induced TRPV1 activation in esophageal mucosa.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- Viewpoints on Acid-induced inflammatory mediators in esophageal mucosa.Journal of neurogastroenterology and motility · 2010Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 4 countries.
Funding
Abstract
Exposure of esophageal mucosa to hydrochloric acid (HCl) is a crucial factor in the pathogenesis of reflux disease. We examined supernatant of HCl-exposed rabbit mucosa for inflammatory mediators enhancing migration of leukocytes and production of H(2)O(2) as an indicator of leukocyte activation. A tubular segment of rabbit esophageal mucosa was tied at both ends to form a sac, which was filled with HCl-acidified Krebs buffer at pH 5 (or plain Krebs buffer as control) and kept oxygenated at 37 degrees C. The medium around the sac (supernatant) was collected after 3 h. Rabbit peripheral blood leukocytes (PBL) were isolated, and sac supernatant was used to investigate PBL migration and H(2)O(2) production. HCl-exposed esophageal mucosa released substance P (SP), CGRP, platelet-activating factor (PAF), and IL-8 into the supernatant. PBL migration increased in response to IL-8 or to supernatant of the HCl-filled mucosal sac. Supernatant-induced PBL migration was inhibited by IL-8 antibodies and by antagonists for PAF (CV3988) or neurokinin 1 (i.e., SP), but not by a CGRP antagonist. Supernatant of the HCl-filled mucosal sac increased H(2)O(2) release by PBL that was significantly reduced by CV3988 and by a SP antagonist but was not affected by IL-8 antibodies or by a CGRP antagonist. We conclude that IL-8, PAF, and SP are important inflammatory mediators released by esophageal mucosa in response to acid that promote PBL migration. In addition, PAF and SP induce production of H(2)O(2) by PBL. These findings provide a direct link between acid exposure and recruitment and activation of immune cells in esophageal mucosa.
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