脂多糖对 IL-33 驱动的原代胃上皮细胞和成纤维细胞再生的干扰。
Interference of LPS with IL-33-Driven Regeneration of Primary Gastric Epithelial Cells and Fibroblasts.
机构信息
Department of Immunology and Infectious Biology, Faculty of Biology and Environmental Protection, Institute of Microbiology, Biotechnology and Immunology, University of Lodz, Banacha Str. 12/16, 90-237 Lodz, Poland.
Department of Microbiology, School of Natural Sciences, National University of Ireland Galway, SW4 Galway, Ireland.
出版信息
Cells. 2021 Jun 4;10(6):1385. doi: 10.3390/cells10061385.
BACKGROUND
Lipopolysaccharide (LPS) of (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 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.
背景
（Hp）细菌的脂多糖（LPS）在体外导致胃组织细胞解体。有人提出白细胞介素（IL）-33 参与胃损伤的愈合。
目的
阐明 Hp LPS 是否会影响 IL-33 引发的胃屏障再生。
方法
用 siRNA IL-33 转染原代胃上皮细胞或成纤维细胞。未暴露或未用 LPS Hp 处理的此类细胞在有或没有外源性 IL-33 的培养基中进行亚培养。然后评估细胞迁移以及氧化应激和细胞凋亡、细胞外信号调节激酶（Erk）的激活、胶原 I 和可溶性 ST2（IL-33 诱饵）的产生。
结果
未用 LPS Hp 处理的对照细胞在存在 IL-33 的情况下迁移。IL-33 的促再生活性与刺激细胞产生胶原 I 有关。即使存在 IL-33，暴露于 LPS Hp 的细胞的伤口愈合也受到抑制。这可能是由于氧化应激和细胞凋亡增加，同时伴随着 Erk 激活、sST2 升高和胶原 I 产生的调节。
结论
由于 LPS Hp 下调了 IL-33 的促再生活性，因此在 Hp 感染期间胃屏障细胞的恢复可能会受到影响。
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