Effect of Lactobacillus gasseri BIO6369 and Lacticaseibacillus rhamnosus BIO5326 on Gastric Carcinogenesis Induced by Helicobacter pylori Infection

IF 4.3 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Helicobacter Pub Date : 2024-07-17 DOI:10.1111/hel.13108

Marine Jauvain, Gorann Lepied, Lucie Bénéjat, Nathalie Roudier, Christelle Dussert, Philippe Lehours, Christine Varon, Emilie Bessède

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Abstract

Background

Helicobacter pylori infection-associated gastric adenocarcinoma is influenced by various factors, including the digestive microbiota. Lactic acid bacteria role in digestive carcinogenesis has been discussed, and some Lactobacillaceae family species have been shown to act against H. pylori-induced inflammation and colonization. However, their effects on H. pylori-related carcinogenesis have not yet been studied. Lactobacillaceae family effects on the epithelial-to-mesenchymal transition (EMT), emergence of cells with cancer stem cell (CSC) properties and the pro-inflammatory response of gastric epithelial cells to H. pylori infection were investigated.

Materials and Methods

A co-culture model of AGS gastric epithelial cells infected with a carcinogenic strain of H. pylori associated with 18 different probiotic strains candidates were used. Different EMT indicators and CSC properties were studied, including quantification of the mesenchymal phenotype, tumorsphere formation, EMT marker expression, and tight junction evaluation with immunofluorescence microscopy. The effect of the strains on the pro-inflammatory response to H. pylori was also evaluated by quantifying interleukin-8 (IL-8) production using ELISA.

Results

Among the strains tested, Lactobacillus gasseri BIO6369 and Lacticaseibacillus rhamnosus BIO5326 induced a 30.6% and 38.4% reduction in the mesenchymal phenotype, respectively, caused a significant decrease in Snail and Zeb1 EMT marker expression and prevented the loss of tight junctions induced by H. pylori infection. A separate co-culture with a Boyden chamber maintained the effects induced by the two strains. H. pylori-induced IL-8 production was also significantly reduced in the presence of L. gasseri BIO6369 and L. rhamnosus BIO5326.

Conclusion

Lactobacillus gasseri BIO6369 and L. rhamnosus BIO5326 strains decreased epithelial-to-mesenchymal transition and inflammation induced by H. pylori infection, suggesting that these species may have a protective effect against H. pylori-induced gastric carcinogenesis.

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加塞乳杆菌 BIO6369 和鼠李糖乳杆菌 BIO5326 对幽门螺旋杆菌感染诱导的胃癌发生的影响

背景：幽门螺杆菌感染相关的胃腺癌受多种因素影响，包括消化道微生物群。乳酸菌在消化系统致癌过程中的作用已被讨论过，一些乳酸菌科菌种已被证明能抑制幽门螺杆菌引起的炎症和定植。然而，它们对幽门螺杆菌相关致癌作用的影响尚未得到研究。本研究探讨了乳酸菌对上皮细胞向间质转化（EMT）、具有癌症干细胞（CSC）特性的细胞的出现以及胃上皮细胞对幽门螺杆菌感染的促炎反应的影响：采用AGS胃上皮细胞与致癌的幽门螺杆菌菌株及18种不同的候选益生菌株共培养模型。研究了不同的 EMT 指标和 CSC 特性，包括间质表型的量化、瘤球的形成、EMT 标记物的表达以及免疫荧光显微镜下的紧密连接评估。此外，还利用 ELISA 定量白细胞介素-8（IL-8）的产生情况，评估了菌株对幽门螺杆菌促炎反应的影响：结果：在测试的菌株中，Lactobacillus gasseri BIO6369和Lacticaseibacillus rhamnosus BIO5326诱导的间质表型分别减少了30.6%和38.4%，导致Snail和Zeb1 EMT标记物表达显著减少，并防止了幽门螺杆菌感染诱导的紧密连接损失。用波登室进行单独的共培养可保持两种菌株诱导的效果。在有 L. gasseri BIO6369 和 L. rhamnosus BIO5326 的情况下，幽门螺杆菌诱导的 IL-8 的产生也显著减少：结论：L. gasseri BIO6369 和 L. rhamnosus BIO5326 菌株可减少幽门螺杆菌感染引起的上皮细胞向间质转化和炎症，这表明这些菌种可能对幽门螺杆菌诱发的胃癌有保护作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Helicobacter 医学-微生物学

CiteScore

8.40

自引率

9.10%

发文量

审稿时长

2 months

期刊介绍： Helicobacter is edited by Professor David Y Graham. The editorial and peer review process is an independent process. Whenever there is a conflict of interest, the editor and editorial board will declare their interests and affiliations. Helicobacter recognises the critical role that has been established for Helicobacter pylori in peptic ulcer, gastric adenocarcinoma, and primary gastric lymphoma. As new helicobacter species are now regularly being discovered, Helicobacter covers the entire range of helicobacter research, increasing communication among the fields of gastroenterology; microbiology; vaccine development; laboratory animal science.