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Response to TNF-α Is Increasing Along with the Progression in Barrett’s Esophagus

Authors
  • Chemnitzer, Olga1
  • Götzel, Katharina1
  • Maurer, Luisa1
  • Dietrich, Arne1, 2
  • Eichfeld, Uwe1
  • Lyros, Orestis1
  • Jansen-Winkeln, Boris1
  • Hoffmeister, Albrecht3
  • Gockel, Ines1
  • Thieme, René1
  • 1 University Medical Center Leipzig, Department of Visceral, Transplant, Thoracic and Vascular Surgery, Liebigstrasse 20, Leipzig, 04103, Germany , Leipzig (Germany)
  • 2 University Medical Center Leipzig, Integrated Research and Treatment Center (IFB) Adiposity Diseases, Philipp-Rosenthal-Strasse 27, Leipzig, 04103, Germany , Leipzig (Germany)
  • 3 University Medical Center Leipzig, Department of Gastroenterology and Rheumatology, Liebigstrasse 20, Leipzig, 04103, Germany , Leipzig (Germany)
Type
Published Article
Journal
Digestive Diseases and Sciences
Publisher
Springer-Verlag
Publication Date
Oct 30, 2017
Volume
62
Issue
12
Pages
3391–3401
Identifiers
DOI: 10.1007/s10620-017-4821-6
Source
Springer Nature
Keywords
License
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Abstract

Background and AimsBarrett’s esophagus, a metaplasia resulting from a long-standing reflux disease, and its progression to esophageal adenocarcinoma (EAC) are characterized by activation of pro-inflammatory pathways, induced by cytokines.MethodsAn in vitro cell culture system representing the sequence of squamous epithelium (EPC1 and EPC2), Barrett’s metaplasia (CP-A), dysplasia (CP-B) to EAC (OE33 and OE19) was used to investigate TNF-α-mediated induction of interleukin-8 (IL-8).ResultsIL-6 and IL-8 expressions are increasing with the progression of Barrett’s esophagus, with the highest expression of both cytokines in the dysplastic cell line CP-B. IL-8 expression in EAC cells was approx. 4.4-fold (OE33) and eightfold (OE19) higher in EAC cells than in squamous epithelium cells (EPC1 and EPC2). The pro-inflammatory cytokine TNF-α increased IL-8 expression in a time-, concentration-, and stage-specific manner. Furthermore, TNF-α changed the EMT marker profile in OE33 cells by decreasing the epithelial marker E-cadherin and increasing the mesenchymal marker vimentin. The anti-inflammatory compound curcumin was able to repress proliferation and to activate apoptosis in both EAC cell lines.ConclusionThe increased basal expression levels of IL-8 with the progression of Barrett’s esophagus constrain NFκB activation and its contribution in the manifestation of Barrett’s esophagus. An anti-inflammatory compound, such as curcumin, could create an anti-inflammatory microenvironment and thus potentially support an increase chemosensitivity in EAC cells.

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