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Mechanisms of peptic ulcer recurrence: role of inflammation

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The mechanism of peptic ulcer recurrence is still unclear. Since ulcerogenic factors such as Helicobacter pylori, non-steroidal anti-inflammatory drugs and stress can increase expression of inflammatory cytokines in gastric mucosa, gastric mucosal inflammation may play key roles in ulcer recurrence. In acetic acid-induced gastric ulcers, persistent infiltration of neutrophils into scarred mucosa, which is caused by prostaglandin deficiency, affects future ulcer recurrence. In a rat model of ulcer recurrence which we developed, inflammatory cytokines such as interleukin (IL)-1β are key mediators of ulcer recurrence. In this model, IL-1β increases expression of adhesion molecules on both leukocytes and endothelial cells, and cytokines, leading to neutrophil infiltration into scarred mucosa. Gastric acid also plays important roles in recurrence of gastric ulcer in this model. Acid regulates inflammatory processes, including expression of adhesion molecules and inflammatory cytokines during ulcer recurrence. This review focuses on recent advances in understanding of the mechanisms underlying development of gastric ulcer recurrence.

10.1163/156856002321544765
/content/journals/10.1163/156856002321544765
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/content/journals/10.1163/156856002321544765
2002-12-01
2016-12-09

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