热不稳定肠毒素促进大肠杆菌对肠上皮细胞的黏附。
Heat-labile enterotoxin promotes Escherichia coli adherence to intestinal epithelial cells.
作者信息
Johnson Amber M, Kaushik Radhey S, Francis David H, Fleckenstein James M, Hardwidge Philip R
机构信息
Center for Infectious Disease Research and Vaccinology, South Dakota State University, Brookings, South Dakota 57007, USA.
出版信息
J Bacteriol. 2009 Jan;191(1):178-86. doi: 10.1128/JB.00822-08. Epub 2008 Oct 31.
Abstract
Given recent evidence suggesting that the heat-labile enterotoxin (LT) provides a colonization advantage for enterotoxigenic Escherichia coli (ETEC) in vivo, we hypothesized that LT preconditions the host intestinal epithelium for ETEC adherence. To test this hypothesis, we used an in vitro model of ETEC adherence to examine the role of LT in promoting bacterium-host interactions. We present data demonstrating that elaboration of LT promotes a significant increase in E. coli adherence. This phenotype is primarily dependent on the inherent ADP-ribosylation activity of this toxin, with a secondary role observed for the receptor-binding LT-B subunit. Rp-3',5'-cyclic AMP (cAMP), an inhibitor of protein kinase A, was sufficient to abrogate LT's ability to promote subsequent bacterial adherence. Increased adherence was not due to changes in the surface expression of the host receptor for the K88ac adhesin. Evidence is also presented for a role for bacterial sensing of host-derived cAMP in promoting adherence to host cells.
摘要
鉴于最近的证据表明热不稳定肠毒素（LT）在体内为产肠毒素大肠杆菌（ETEC）提供了定殖优势，我们推测LT使宿主肠道上皮细胞对ETEC的黏附产生预处理。为了验证这一假设，我们使用了ETEC黏附的体外模型来研究LT在促进细菌与宿主相互作用中的作用。我们提供的数据表明，LT的释放显著促进了大肠杆菌的黏附。这种表型主要依赖于该毒素固有的ADP核糖基化活性，而受体结合性LT-B亚基起次要作用。蛋白激酶A的抑制剂Rp-3',5'-环磷酸腺苷（cAMP）足以消除LT促进后续细菌黏附的能力。黏附增加并非由于宿主K88ac黏附素受体的表面表达发生变化。还有证据表明，细菌感知宿主来源的cAMP在促进对宿主细胞的黏附中起作用。
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