ZT：哪些幽门螺杆菌菌株具有更高的致胃癌风险？哪些也许有益？

来源: fuz 于 2019-11-15 02:45:14 [档案] [博客] [旧帖] [给我悄悄话] 本文已被阅读：次 (17618 bytes)

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http://www.medsky.cn/meida/chaoliu/269.html

幽门螺杆菌的特征是具有高度的种内遗传多样性。不同地区人群所感染的幽门螺杆菌菌株不仅在单个基因的序列上有差异，而且表现出基因含量和染色体组织的差异……

感染了含有CagA、s1类型VacA和BabA的幽门螺杆菌菌株的人群，其发生胃癌的风险最高。幽门螺杆菌与胃癌风险相关，且不同类型幽门螺杆菌菌株与胃癌的相关性具有显著差异。………

http://www.mdweekly.com.cn/html/xueshu/huiyizhongxin/2019/0819/22916.html

不同角度看幽门螺杆菌

越来越多的研究显示，Hp对人体可能存在的保护作用，并且一些研究也反映了根除后会出现的一些问题，包括：Hp实际上是一种与人体共生的有益细菌，被根除后会破坏肠道菌群生态平衡；在发展中国家，携带Hp的孩子更不容易患上过敏；儿童时期，携带Hp可以降低哮喘的发病风险；携带Hp可以降低湿疹的发生率；当Hp从人体的胃中消失后，人们更容易患上胃食管反流病及其并发症（调查显示，当Hp被根除及胃癌发病率下降同时，食管腺癌的发病率在几十年后开始上升），比如巴雷特食管和食管腺癌，也更容易体重增加等。此外，2013年的一项研究显示，根除Hp带来多种不良后果：50%以上的患者在根除中会出现不良反应；20%作用的概率会根除失败；根除后肠道菌群的变化可能带来长期的健康影响；使用抗生素会增加耐药性细菌产生的风险。………

http://sph.54doctors.net/Html/News/Articles/3830.html

　中国人群幽门螺杆菌（Hp）感染率很高达到50%以上，而且一旦感染后如不进行针对治疗，很难自然根除。很多人一旦悉知自身感染了Hp就会感觉体内安放了一枚能让人患胃病甚至是胃癌的“不定时炸弹”。可大多数人感染了Hp却终身没有胃病的发生。随着科学向前深入，发现Hp分为不同类型，Hp菌株基因甚至能起到对我们人类有益菌的作用，而另一些Hp则会让我们患病的几率大大增强。

　　研究发现，患有Hp的病人如果不进行分型检测，而是选择一旦发现Hp，不论有无症状都进行根除，那么我们一定要认识到根除本身会带来很多意想不到的副作用。近十年来随着我们大规模杀死Hp，远端胃癌发病率下降的很快，然而我们惊讶的发现，近端胃癌却呈现快速的高增长率，我们逐渐认识到Hp其实也许对我们人类起到一定保护作用。

https://www.ncbi.nlm.nih.gov/pubmed/30455363

Within human stomachs, RABEP2 and G3BP2 expression in gastric epithelium increased in parallel with the severity of premalignant and malignant lesions and was significantly elevated in intestinal metaplasia and dysplasia, as well as gastric adenocarcinoma, compared with gastritis alone. These results indicate that carcinogenic strains of H. pylori induce dramatic and specific changes within the gastric proteome in vivo and that a subset of altered proteins within pathways with oncogenic potential may facilitate the progression of gastric carcinogenesis in humans.

https://www.nature.com/articles/s41598-018-34425-4

Isolation of less pathogenic H. pylori strains carrying CagA with attenuated pathobiological activity in a small and isolated host population is reminiscent of the result of our previous study regarding v225d CagA, a natural CagA variant of H. pylori isolated from an Amerindian subject living in the Amazon rainforest54. Like Hp_TH2099 CagA, v225d CagA was also incapable of binding with PAR1b, suggesting that attenuated CagA activity, especially loss of PAR1b binding, is a hallmark of H. pylori sustainably cohabiting with a small number of hosts. Although it needs to be determined whether macaques carry and transmit H. pylori among themselves in wild life, many studies have shown that wild macaques have an intimate relationship with humans, especially in Asian countries55,56. It is possible that macaques became infected with H. pylori from human vomit or waste. Conversely, humans might have acquired H. pylorifrom macaques by feeding on them, a human habit that has been historically recorded in many geographic regions of the world. It is tempting to speculate that rapid evolution of distinct H. pylorisubpopulations has been made possible by back and forth natural infection/colonization between humans and non-human primates, which may have facilitated bacterial microevolutions in a way that is milder than the mutation burst triggered by experimental H. pyloriinfection.