1. Interference of LPS H. pylori with IL-33-Driven Regeneration of Caviae porcellus Primary Gastric Epithelial Cells and Fibroblasts.
- Author
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Gonciarz W, Krupa A, Moran AP, Tomaszewska A, and Chmiela M
- Subjects
- Animals, Guinea Pigs, Lipopolysaccharides chemistry, Epithelial Cells metabolism, Fibroblasts metabolism, Gastric Mucosa physiology, Helicobacter pylori chemistry, Interleukin-33 metabolism, Lipopolysaccharides pharmacology, Regeneration drug effects
- 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.
- Published
- 2021
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