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牙龈卟啉单胞菌通过铁死亡促进酒精性肝病的发生。

Porphyromonas gingivalis as a promotor in the development of the alcoholic liver disease via ferroptosis.

机构信息

Department of Prothodontics, Shanghai Stomatological Hospital, Fudan University, Shanghai, China; Shanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Fudan University, Shanghai, China; Medical College, Anhui University of Science and Technology, Huainan, China; Department of Stomatology, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.

Department of Stomatology, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.

出版信息

Microbes Infect. 2024 Mar-Apr;26(3):105250. doi: 10.1016/j.micinf.2023.105250. Epub 2023 Nov 13.

Abstract

Alcoholic liver disease (ALD) is a liver disease caused by heavy drinking. Porphyromonas gingivalis (P.g), a major cause of periodontitis, whose antibodies are elevated in severe ALD patients in the plasma. The purpose of this study is to further study the role and the molecular mechanism of P.g in the progress of ALD. In this study, saliva of patients with ALD was collected. Then, an animal model of ALD with oral P.g administration was established, pathology of liver and spleen, intestinal microorganisms and metabolites were analyzed. The molecular mechanism of P.g on ALD was analyzed in vitro. ALD and intestinal microflora and metabolite changes were observed more serious in the alcohol and P.g groups than the alcohol group. Moreover, ferroptosis was aggravated by P.g in the liver. Meanwhile, P.g promoted ferroptosis accomplication with alcohol in vitro, which can be reversed by ferroptosis inhibitors. In conclusion, P.g aggravates ALD through exacerbation gut microbial metabolic disorder in mice with alcohol, which maybe depend on ferroptosis activation in hepatocytes. The study provides a new strategy for prevention and treatment of ALD by improving the oral micro-environment.

摘要

酒精性肝病(ALD)是由大量饮酒引起的肝脏疾病。牙龈卟啉单胞菌(P.g)是牙周炎的主要病因,其抗体在严重 ALD 患者的血浆中升高。本研究旨在进一步研究 P.g 在 ALD 进展中的作用和分子机制。本研究收集了 ALD 患者的唾液。然后,建立了口服 P.g 给药的 ALD 动物模型,分析了肝脏和脾脏的病理学、肠道微生物和代谢物。在体外分析了 P.g 对 ALD 的分子机制。与酒精组相比,酒精和 P.g 组的 ALD 和肠道微生物群和代谢物变化更严重。此外,P.g 在肝脏中加重了铁死亡。同时,P.g 在体外促进了酒精引起的铁死亡并发症,铁死亡抑制剂可逆转这一过程。总之,P.g 通过加重酒精诱导的小鼠肠道微生物代谢紊乱加重 ALD,这可能依赖于肝细胞中铁死亡的激活。该研究为通过改善口腔微环境预防和治疗 ALD 提供了新策略。

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