向胃病倾斜：宿主-病原体基因组错配？
Tipping the Scale Toward Gastric Disease: A Host-Pathogen Genomic Mismatch?
作者信息
Tavera Gloria, Morgan Douglas R, Williams Scott M
机构信息
Department of Population and Quantitative Health Sciences, Case Western Reserve University, Cleveland, OH, USA.
Vanderbilt Ingram Cancer Center, Nashville, Tennessee.
出版信息
Curr Genet Med Rep. 2018 Dec;6(4):199-207. doi: 10.1007/s40142-018-0153-x. Epub 2018 Oct 10.
PURPOSE OF REVIEW
Chronic infection with infection is necessary but not sufficient to initiate development of intestinal-type gastric adenocarcinoma. It is not clear what additional factors tip the scale from commensal bacteria towards a pathogen that facilitates development of gastric cancer. Genetic variants in both the pathogen and host have been implicated, but neither alone explains a substantial portion of disease risk.
RECENT FINDINGS
In this review, we consider studies that address the important role of human and bacterial genetics, ancestry and their interactions in determining gastric disease risk. We observe gaps in the current literature that should guide future work to confirm the hypothesis of the interacting roles of host and bacterial genetics that will be necessary to translate these findings into clinically relevant information.
SUMMARY
We summarize genetic risk factors for gastric disease in both and human hosts. However, genetic variation of one or the other organism in isolation insufficiently explains gastric disease risk. The most promising models of gastric disease risk simultaneously consider the genetic variation of both the and human host, under a co-evolution model.
综述目的
幽门螺杆菌慢性感染是肠型胃腺癌发生发展的必要但非充分条件。尚不清楚哪些额外因素会使共生菌转变为促进胃癌发生的病原体。病原体和宿主的基因变异都与之相关，但单独任何一方都不能解释很大一部分疾病风险。
最新发现
在本综述中，我们考量了一些研究，这些研究探讨了人类和细菌遗传学、血统及其相互作用在决定胃部疾病风险方面的重要作用。我们发现当前文献中存在空白，这些空白应指导未来的研究工作，以证实宿主和细菌遗传学相互作用的假说，而这对于将这些发现转化为临床相关信息是必要的。
总结
我们总结了幽门螺杆菌和人类宿主中胃部疾病的遗传风险因素。然而，单独一种生物体的基因变异不足以解释胃部疾病风险。在共同进化模型下，最有前景的胃部疾病风险模型同时考虑幽门螺杆菌和人类宿主的基因变异。
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