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粘附蛋白HopQ与胃上皮细胞中人类细胞表面粘附分子CEACAMs之间的致病相互作用。

Pathogenic interactions between adhesion protein HopQ and human cell surface adhesion molecules CEACAMs in gastric epithelial cells.

作者信息

Xia Ran, Zhang Bo, Wang Xinxin, Jia Qiuying

机构信息

Geriatrics Department, the Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, China.

Medical Record Room, the Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, China.

出版信息

Iran J Basic Med Sci. 2019 Jul;22(7):710-715. doi: 10.22038/ijbms.2019.34237.81.

Abstract

OBJECTIVES

The present paper aims to review the studies describing the interactions between HopQ and CEACAMs along with possible mechanisms responsible for pathogenicity of .

MATERIALS AND METHODS

The literature was searched on "PubMed" using different key words including , CEACAM and gastric.

RESULTS

HopQ is one of the outer membrane proteins of and belongs to the family of adhesin proteins. In contrast to other adhesins, HopQ interacts with host cell surface molecules in a glycan independent manner. Human CEACAMs are the cell surface adhesion molecules mainly present on the epithelial cells, endothelial cells and leukocytes. The overexpression of these molecules may contribute to cancer progression and relapse. Recent studies have shown that HopQ may interact with human CEACAMs, particularly CEACAM1, CEACAM3, CEACAM5 and CEACAM6, but not CEACAM8. HopQ interacts with GFCC'C" interaction surface of IgV domain of N- terminal region of CEACAM1. Moreover, binding of HopQ to CEACAM1 prevent its trans-dimerization and stabilizes it in monomeric form. may use these HopQ-CEACAM interactions to transfer its CagA oncoprotein into host gastric epithelial cells, which is followed by its phosphorylation and release of interleukin-8. HopQ-CEACAM interactions may also utilize T4SS, instead of CagA, to activate NF-κB signaling and trigger inflammation.

CONCLUSION

HopQ of may interact with CEACAMs of the human gastric cells to induce the development of gastric ulcers and cancers by transferring CagA oncoprotein or inducing activation of T4SS to initiate and maintain inflammatory reactions.

摘要

目的

本文旨在综述描述HopQ与癌胚抗原相关细胞黏附分子(CEACAMs)之间相互作用的研究,以及探讨其致病机制。

材料与方法

在“PubMed”上使用包括CEACAM和胃等不同关键词进行文献检索。

结果

HopQ是幽门螺杆菌的外膜蛋白之一,属于黏附素蛋白家族。与其他黏附素不同,HopQ以不依赖聚糖的方式与宿主细胞表面分子相互作用。人CEACAMs是主要存在于上皮细胞、内皮细胞和白细胞上的细胞表面黏附分子。这些分子的过度表达可能促进癌症进展和复发。最近的研究表明,HopQ可能与人CEACAMs相互作用,特别是CEACAM1、CEACAM3、CEACAM5和CEACAM6,但不与CEACAM8相互作用。HopQ与CEACAM1 N端区域IgV结构域的GFCC'C''相互作用表面相互作用。此外,HopQ与CEACAM1的结合可防止其反式二聚化,并使其稳定在单体形式。幽门螺杆菌可能利用这些HopQ-CEACAM相互作用将其CagA癌蛋白转移到宿主胃上皮细胞中,随后其磷酸化并释放白细胞介素-8。HopQ-CEACAM相互作用也可能利用四型分泌系统(T4SS),而不是CagA,来激活NF-κB信号并引发炎症。

结论

幽门螺杆菌的HopQ可能与人胃细胞的CEACAMs相互作用,通过转移CagA癌蛋白或诱导T4SS激活来引发和维持炎症反应,从而导致胃溃疡和癌症的发生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f51/7196344/246fcd3841b9/IJBMS-22-710-g001.jpg

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