Abstract
Background: Lipopolysaccharide (LPS) of Helicobacter pylori (Hp) bacteria causes disintegration of gastric tissue cells in vitro. It has been suggested that interleukin (IL)-33 is involved in healing gastric injury. Aim: To elucidate whether Hp LPS affects regeneration of gastric barrier initiated by IL-33. Methods: Primary gastric epithelial cells or fibroblasts from Caviae porcellus were transfected with siRNA IL-33. Such cells, not exposed or treated with LPS Hp, were sub-cultured in the medium with or without exogenous IL-33. Then cell migration was assessed in conjunction with oxidative stress and apoptosis, activation of extracellular signal-regulated kinase (Erk), production of collagen I and soluble ST2 (IL-33 decoy). Results: Control cells not treated with LPS Hp migrated in the presence of IL-33. The pro-regenerative activity of IL-33 was related to stimulation of cells to collagen I production. Wound healing by cells exposed to LPS Hp was inhibited even in the presence of IL-33. This could be due to increased oxidative stress and apoptosis in conjunction with Erk activation, sST2 elevation and modulation of collagen I production. Conclusions: The recovery of gastric barrier cells during Hp infection potentially can be affected due to downregulation of pro-regenerative activity of IL-33 by LPS Hp.
Highlights
Statistical analysis was performed using the nonparametric Mann-Whitney U test at p < 0.05. * cells exposed to LPS H. pylori in medium without IL-33 vs. cells exposed to LPS H. pylori with significance at p < 0.05. * cells exposed to LPS H. pylori in medium without IL-33 vs. cells exin medium with IL-33; n cells not treated with LPS H. pylori, sub-cultured in medium without IL-33 posed to LPS H. pylori in medium with IL-33;
Our study showed that LPS H. pylori may initiate deleterious effects towards gastric barrier cells due to increasing oxidative stress and apoptosis in conjunction with elevated production of caspases, might potentially be upregulated by metalloproteinase (MMP)-9 and sST2
Our study showed that LPS H. pylori may initiate deleterious effects towards gastric barrier cells due to increasing oxidative stress and apoptosis in conjunction with elevated production of caspases and sST2
Summary
Ten to fifteen percent of H. pylori-infected individuals will develop chronic inflammatory response, which increases the risk of gastric and duodenal ulcers, stomach cancer and mucosa associated lymphoid tissue (MALT) lymphoma [2,3,4]. Among cell-bound components, H. pylori LPS is involved in gastric tissue destruction and development of inflammatory response. Methods: Primary gastric epithelial cells or fibroblasts from Caviae porcellus were transfected with siRNA IL-33. Such cells, not exposed or treated with LPS Hp, were sub-cultured in the medium with or without exogenous IL-33. Cell migration was assessed in conjunction with oxidative stress and apoptosis, activation of extracellular signal-regulated kinase (Erk), production of collagen
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