卡加
细菌粘附素
分泌物
幽门螺杆菌
生物
受体
细菌外膜
糖基化
毒力因子
细胞生物学
微生物学
毒力
基因
生物化学
遗传学
大肠杆菌
作者
Verena Königer,Lea Holsten,Ute Harrison,Benjamin Busch,Eva Loell,Qing Zhao,Daniel A. Bonsor,Alexandra Roth,Arnaud Kengmo Tchoupa,Stella I. Smith,Susanna Mueller,Eric J. Sundberg,Wolfgang Zimmermann,Wolfgang Fischer,Christof R. Hauck,Rainer Haas
出处
期刊:Nature microbiology
日期:2016-10-17
卷期号:2 (1)
被引量:132
标识
DOI:10.1038/nmicrobiol.2016.188
摘要
Helicobacter pylori (Hp) strains that carry the cag type IV secretion system (cag-T4SS) to inject the cytotoxin-associated antigen A (CagA) into host cells are associated with peptic ulcer disease and gastric adenocarcinoma. CagA translocation by Hp is mediated by β1 integrin interaction of the cag-T4SS. However, other cellular receptors or bacterial outer membrane adhesins essential for this process are unknown. Here, we identify the HopQ protein as a genuine Hp adhesin, exploiting defined members of the carcinoembryonic antigen-related cell adhesion molecule family (CEACAMs) as host cell receptors. HopQ binds the amino-terminal IgV-like domain of human CEACAM1, CEACAM3, CEACAM5 or CEACAM6 proteins, thereby enabling translocation of the major pathogenicity factor CagA into host cells. The HopQ-CEACAM interaction is characterized by a remarkably high affinity (KD from 23 to 268 nM), which is independent of CEACAM glycosylation, identifying CEACAMs as bona fide protein receptors for Hp. Our data suggest that the HopQ-CEACAM interaction contributes to gastric colonization or Hp-induced pathologies, although the precise role and functional consequences of this interaction in vivo remain to be determined.
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