Chronic Infection With Gastric Helicobacters Induces Hepatic Lesions in Mice

IF 4.3 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Helicobacter Pub Date : 2025-04-10 DOI:10.1111/hel.70032

Lornella Seeneevassen, Elodie Sifré, Sadia Khalid, Mathilde Managau, Francis Mégraud, Armelle Ménard, Pierre Dubus, Pirjo Spuul, Christine Varon

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Abstract

Background

Helicobacter pylori infection is one of the most prevalent chronic bacterial infections worldwide. This bacillus colonizes the human stomach lifelong, where it induces chronic gastritis, evolving in some cases to gastro-duodenal ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. H. pylori infection has also been associated with extragastric diseases, and clinical data have suggested a role in liver pathogenesis. This retrospective study evaluated the consequences of chronic infection with gastric Helicobacters on liver pathogenesis in a mouse experimental model.

Materials and Methods

C57BL6 mice were infected with either H. felis (n = 12) or five human and mouse-adapted strains of H. pylori (n = 77) for one year. Uninfected mice were used as negative controls (n = 10). Histopathological analysis of paraffin-embedded liver tissue sections was performed, and scores were determined in a double-blind manner for inflammation and steatosis.

Results

Mice infected with H. felis and several H. pylori strains developed more liver parenchymal inflammation and steatosis, known precursor lesions of liver carcinogenesis, compared to non-infected mice. The presence of liver lesions was positively correlated with the detection of lesions of the gastric mucosa, more particularly gastric inflammation and metaplasia.

Conclusion

Chronic infection of mice with H. felis and H. pylori induces liver pathogenesis characterized by parenchymal inflammation and steatosis, which may be associated with the severity of gastric histopathological lesions. Understanding H. pylori infection's impact on extragastric lesions could in fine help detect and prevent the emergence of other digestive tract-related diseases.

Abstract Image

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慢性幽门螺杆菌感染诱导小鼠肝脏病变

背景幽门螺杆菌感染是世界上最常见的慢性细菌感染之一。这种芽孢杆菌终生在人的胃中定植，引起慢性胃炎，在某些情况下演变为胃十二指肠溃疡、胃腺癌和粘膜相关淋巴组织淋巴瘤。幽门螺杆菌感染也与胃外疾病有关，临床资料表明其在肝脏发病机制中起作用。本回顾性研究在小鼠实验模型中评估了慢性胃幽门螺杆菌感染对肝脏发病机制的影响。材料与方法C57BL6小鼠分别感染12株猫毛杆菌（n = 12）和77株人鼠型幽门螺杆菌（n = 77），时间为1年。未感染小鼠作为阴性对照（n = 10）。对石蜡包埋的肝组织切片进行组织病理学分析，并以双盲方式确定炎症和脂肪变性的评分。结果与未感染的小鼠相比，感染猫芽孢杆菌和几种幽门螺旋杆菌的小鼠发生更多的肝实质炎症和脂肪变性，这是已知的肝癌发生的前体病变。肝脏病变的存在与胃粘膜病变的检出率呈正相关，尤其是胃炎症和化生。结论慢性感染猫芽孢杆菌和幽门螺旋杆菌可引起肝脏实质炎症和脂肪变性，并可能与胃组织病理病变的严重程度有关。了解幽门螺杆菌感染对胃外病变的影响，有助于发现和预防其他消化道相关疾病的发生。

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.