ArticleJournal of gastroenterology2014
Toll-like receptor 4 activation in Barrett's esophagus results in a strong increase in COX-2 expression.
Article in Journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 58 citations in OpenAlex.
- Intratumoral microbiome: the double-edged sword in remodeling cancer immunotherapy.Molecular cancer · 2026Review
- Signaling pathways and targeted interventions for precancers.Signal transduction and targeted therapy · 2026Review
- Intestinal and esophageal microbiota in esophageal cancer development and treatment.Gut microbes · 2025Review
- Unveiling the role of m6A modification in esophageal cancer: a new frontier in tumor innate interferon immunity.Cancer cell international · 2025Review
- A Role for High Mobility Group Box 1 (HMGB1) Release in the Pathogenesis of Gastroesophageal Reflux Disease.Neurogastroenterology and motility · 2025Article
- The role of the esophageal and intestinal microbiome in gastroesophageal reflux disease: past, present, and future.Frontiers in immunology · 2025Review
- Altered Microbiome Promotes Pro-Inflammatory Pathways in Oesophago-Gastric Tumourigenesis.Cancers · 2024Review
- Mechanistic Insights on Microbiota-Mediated Development and Progression of Esophageal Cancer.Cancers · 2024Review
- Prebiotic proanthocyanidins inhibit bile reflux-induced esophageal adenocarcinoma through reshaping the gut microbiome and esophageal metabolome.JCI insight · 2024Article
- From microbes to medicine: harnessing the power of the microbiome in esophageal cancer.Frontiers in immunology · 2024Review
- Herbal melanin modulates PGE2 and IL-6 gastroprotective markers through COX-2 and TLR4 signaling in the gastric cancer cell line AGS.BMC complementary medicine and therapies · 2023Article
- Intersections between innate immune response and gastric cancer development.World journal of gastroenterology · 2023Review
- Endotoxemia and Gastrointestinal Cancers: Insight into the Mechanisms Underlying a Dangerous Relationship.Microorganisms · 2023Review
- Analysis of the gut microbiota in children with gastroesophageal reflux disease using metagenomics and metabolomics.Frontiers in cellular and infection microbiology · 2023Article
- Mechanisms and pathophysiology of Barrett oesophagus.Nature reviews. Gastroenterology & hepatology · 2022Review
- Oral Microbiota Variation: A Risk Factor for Development and Poor Prognosis of Esophageal Cancer.Digestive diseases and sciences · 2022Review
- Cross-talk between the microbiome and chronic inflammation in esophageal cancer: potential driver of oncogenesis.Cancer metastasis reviews · 2022Review
- COX-2 strengthens the effects of acid and bile salts on human esophageal cells and Barrett esophageal cells.BMC molecular and cell biology · 2022Article
- Pathophysiology of reflux oesophagitis: role of Toll-like receptors 2 and 4 and Farnesoid X receptor.Virchows Archiv : an international journal of pathology · 2021Article
- Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBarrett's esophagus (BE) is known to progress to esophageal adenocarcinoma in a setting of chronic inflammation. Toll-like receptor (TLR) 4 has been linked to inflammation-associated carcinogenesis. We aimed to determine the expression and functional activity of TLR4 in the esophagus and whether TLR4 activation in BE could promote carcinogenesis by inducing COX-2 expression.
methodsTLR4 expression in esophageal adenocarcinoma, BE, duodenum, reflux esophagitis and normal squamous esophagus biopsies was assessed using real-time PCR and validated by in situ hybridization and immunohistochemistry. Ex vivo cultures of BE, duodenum and normal squamous esophagus biopsies and a BE cell line (BAR-T) were stimulated with the TLR4 agonist lipopolysaccharide (LPS). To evaluate the effect of TLR4 activation, NF-κB activation, IL8 secretion and expression and COX-2 expression were determined.
resultsTLR4 expression was significantly increased in esophageal adenocarcinoma, BE, duodenum and reflux esophagitis compared to normal squamous esophagus. LPS stimulation resulted in NF-κB activation and a dose-dependent increase of IL8 secretion and mRNA expression. The induction of IL8 was more evident in BE compared to normal squamous esophagus. Upon LPS stimulation, COX-2 expression increased significantly in ex vivo cultured BE biopsies, which was observed in both epithelium and lamina propria cells. However, no effect was found in duodenum and normal squamous esophagus biopsies.
conclusionTLR4 activation in BE results in a strong increase in COX-2 and may contribute to malignant transformation.
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