Abstract
Recent reports have demonstrated significantly higher expression levels of interleukin-8 (IL-8) in patients with gastroesophageal reflux disease (GERD) including non-erosive reflux disease (NERD). The levels of IL-8 mRNA expression were significantly decreased after proton pump inhibitor. The esophageal expression of CINCs, rat IL-8-like chemokines, was markedly enhanced in the models of acute or chronic esophagitis in rats. The production of IL-8 from esophageal mucosal cells was enhanced by the exposure to bile acid. These results suggest that IL-8 chemokine may play a major role in the pathogenesis of esophageal inflammation in GERD.
MeSH terms
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Animals
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Barrett Esophagus / etiology
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Bile Acids and Salts / adverse effects
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Chemokines, CXC / genetics
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Chemokines, CXC / metabolism
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Depression, Chemical
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Disease Models, Animal
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Enzyme Inhibitors / pharmacology
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Enzyme Inhibitors / therapeutic use
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Esophagitis, Peptic / etiology
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Esophagus / metabolism
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Gastroesophageal Reflux / drug therapy
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Gastroesophageal Reflux / etiology*
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Gastroesophageal Reflux / metabolism
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Gene Expression
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Humans
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Inflammation Mediators / metabolism*
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Intercellular Signaling Peptides and Proteins / genetics
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Intercellular Signaling Peptides and Proteins / metabolism
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Interleukin-8 / genetics
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Interleukin-8 / metabolism*
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Mucous Membrane / metabolism
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Proton Pump Inhibitors
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RNA, Messenger / metabolism
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Rats
Substances
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Bile Acids and Salts
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Chemokines, CXC
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Enzyme Inhibitors
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Inflammation Mediators
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Intercellular Signaling Peptides and Proteins
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Interleukin-8
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Proton Pump Inhibitors
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RNA, Messenger