Modeling Lipopolysaccharide-Elicited Inflammation Using 3D Mouse Gastric Organoids.

IF 3.1 3区生物学 Q3 CELL BIOLOGY

Cell Biology International Pub Date : 2025-08-05 DOI:10.1002/cbin.70066

Aoqing Xu, Xiyu Wang, Zhifan Ye, Tao Li, Fengrui Yang, McKay Mullen, Xia Ding, Xing Liu, Zhikai Wang

引用次数: 0

Abstract

Colonization of Helicobacter pylori (H. pylori) in stomach often causes gastritis, an inflammation of the stomach lining that is closely associated with serious conditions like ulcers and gastric cancer. Of the toxicity mechanisms, microbial lipopolysaccharide (LPS) binding to TLR4 receptor on the glandular cells activates the NF-κB pathway, inducing pro-inflammatory cytokine release and immune cell infiltration, which results in the tissue damage. However, whether LPS has any direct damaging effect on gastric epithelial cells has been in debate. By using mouse gastric organoids that were grown from the isolated glands and maintained the cellular compositions, we demonstrate various effects of variable LPS concentrations on the glandular epithelial cells, including mild promotion of cell proliferation at the low concentration and induced loss of cell polarity and altered gene expressions at the high concentration. These findings provide insights into how LPS directly affects the stomach lining.

查看原文本刊更多论文

用三维小鼠胃类器官模拟脂多糖引起的炎症。

幽门螺杆菌（Helicobacter pylori, h.p ylori）在胃里的定植经常导致胃炎，这是一种胃粘膜炎症，与溃疡和胃癌等严重疾病密切相关。在其毒性机制中，微生物脂多糖（microbial lipopolaccharide， LPS）与腺体细胞上的TLR4受体结合，激活NF-κB通路，诱导促炎细胞因子释放和免疫细胞浸润，导致组织损伤。然而，脂多糖是否对胃上皮细胞有直接的损伤作用一直存在争议。通过使用从离体腺体生长并维持细胞成分的小鼠胃类器官，我们证明了不同浓度的LPS对腺上皮细胞的各种影响，包括低浓度时轻度促进细胞增殖，高浓度时诱导细胞极性丧失和基因表达改变。这些发现为LPS如何直接影响胃粘膜提供了见解。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Cell Biology International 生物-细胞生物学

CiteScore

7.60

自引率

0.00%

发文量

208

审稿时长

1 months

期刊介绍： Each month, the journal publishes easy-to-assimilate, up-to-the minute reports of experimental findings by researchers using a wide range of the latest techniques. Promoting the aims of cell biologists worldwide, papers reporting on structure and function - especially where they relate to the physiology of the whole cell - are strongly encouraged. Molecular biology is welcome, as long as articles report findings that are seen in the wider context of cell biology. In covering all areas of the cell, the journal is both appealing and accessible to a broad audience. Authors whose papers do not appeal to cell biologists in general because their topic is too specialized (e.g. infectious microbes, protozoology) are recommended to send them to more relevant journals. Papers reporting whole animal studies or work more suited to a medical journal, e.g. histopathological studies or clinical immunology, are unlikely to be accepted, unless they are fully focused on some important cellular aspect. These last remarks extend particularly to papers on cancer. Unless firmly based on some deeper cellular or molecular biological principle, papers that are highly specialized in this field, with limited appeal to cell biologists at large, should be directed towards journals devoted to cancer, there being very many from which to choose.