We are analyzing https://link.springer.com/article/10.1007/s00535-013-0862-6.

Title:
Toll-like receptor 4 activation in Barrett’s esophagus results in a strong increase in COX-2 expression | Journal of Gastroenterology
Description:
Background Barrett’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. Methods TLR4 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. Results TLR4 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. Conclusion TLR4 activation in BE results in a strong increase in COX-2 and may contribute to malignant transformation.
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pubmed, article, google, scholar, cas, esophagus, barretts, tolllike, central, tlr, expression, receptor, cell, esophageal, adenocarcinoma, cancer, squamous, van, cox, activation, receptors, biol, gastroenterology, human, normal, signaling, epithelial, utrecht, lipopolysaccharide, access, oesophagus, cyclooxygenase, gut, immunol, intestinal, gastroenterol, netherlands, results, siersema, reflux, esophagitis, cells, gastric, protein, tollip, zhang, university, medical, center, privacy,

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month download article/chapter inflammation-metaplasia-dysplasia-adenocarcinoma sequence recruit ubiquitin-conjugated proteins decreased toll-interacting protein amide-linked acyl chains abdel-latif mm produce anti-microbial peptides metaplasia-dysplasia-adenocarcinoma sequence large population-based study real-time pcr related subjects van sandick jw nuclear factor-kappab pathway enhances tlr2-mediated responses full article pdf leptospira interrogans lipid lps-induced tlr4 signaling tlr3-mediated nf-{kappa} upper gastrointestinal tract il-1ri pathway gene expression profiles kees fluiter privacy choices/manage cookies lamina propria cells nuclear factor kappa proton pump inhibitors sporadic colorectal adenomas cell physiol biochem experimental animal model academic medical center reduces cell proliferation cell wall components immune cell composition natl cancer inst abreu mt proton pump inhibitor normal squamous esophagus check access instant access md-2 enables toll van deventer sj van noort jm human subjects oxidative dna damage upper gastrointestinal toxicity clin cancer res inflammation driven esophageal nat cell biol cyclooxygenase-2 mediated regulation de boer ag

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Endogenous ligands of TLR2 and TLR4: agonists or assistants?
Esophageal adenocarcinoma incidence: are we reaching the peak?
Why is the high grade inhibition of gastric acid secretion afforded by proton pump inhibitors often required for healing of reflux esophagitis?

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         description:Barrett’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. TLR4 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. TLR4 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. TLR4 activation in BE results in a strong increase in COX-2 and may contribute to malignant transformation.
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      description:Barrett’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. TLR4 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. TLR4 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. TLR4 activation in BE results in a strong increase in COX-2 and may contribute to malignant transformation.
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         Abdominal Surgery
         Colorectal Surgery
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