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幽门螺杆菌诱导的胃外细胞过早衰老可能导致慢性皮肤病。

Helicobacter pylori-induced premature senescence of extragastric cells may contribute to chronic skin diseases.

作者信息

Lewinska Anna, Wnuk Maciej

机构信息

Department of Genetics, University of Rzeszow, Werynia 502, 36-100, Kolbuszowa, Poland.

出版信息

Biogerontology. 2017 Apr;18(2):293-299. doi: 10.1007/s10522-017-9676-x. Epub 2017 Jan 10.

DOI:10.1007/s10522-017-9676-x
PMID:28074309
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5350214/
Abstract

Helicobacter pylori, one of the most frequently observed bacterium in the human intestinal flora, has been widely studied since Marshall and Warren documented a link between the presence of H. pylori in the gastrointestinal tract and gastritis and gastric ulcers. Interestingly, H. pylori has also been found in several other epithelial tissues, including the eyes, ears, nose and skin that may have direct or indirect effects on host physiology and may contribute to extragastric diseases, e.g. chronic skin diseases. More recently, it has been shown that H. pylori cytotoxin CagA expression induces cellular senescence of human gastric nonpolarized epithelial cells that may lead to gastrointestinal disorders and systemic inflammation. Here, we hypothesize that also chronic skin diseases may be promoted by stress-induced premature senescence (SIPS) of skin cells, namely fibroblasts and keratinocytes, stimulated with H. pylori cytotoxins. Future studies involving cell culture models and clinical specimens are needed to verify the involvement of H. pylori in SIPS-based chronic skin diseases.

摘要

幽门螺杆菌是人类肠道菌群中最常见的细菌之一,自马歇尔和沃伦记录了胃肠道中幽门螺杆菌的存在与胃炎和胃溃疡之间的联系以来,它就受到了广泛研究。有趣的是,在包括眼睛、耳朵、鼻子和皮肤在内的其他几种上皮组织中也发现了幽门螺杆菌,这些组织可能对宿主生理有直接或间接影响,并可能导致胃外疾病,如慢性皮肤病。最近的研究表明,幽门螺杆菌细胞毒素CagA的表达会诱导人胃非极化上皮细胞的细胞衰老,这可能导致胃肠道疾病和全身炎症。在这里,我们假设,幽门螺杆菌细胞毒素刺激皮肤细胞(即成纤维细胞和角质形成细胞)的应激诱导早衰(SIPS)也可能促进慢性皮肤病。未来需要进行涉及细胞培养模型和临床标本的研究,以验证幽门螺杆菌在基于SIPS的慢性皮肤病中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d1/5350214/f28d08c13091/10522_2017_9676_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d1/5350214/f28d08c13091/10522_2017_9676_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d1/5350214/f28d08c13091/10522_2017_9676_Fig1_HTML.jpg

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