Anthrax edema toxin inhibits Nox1-mediated formation of reactive oxygen species by colon epithelial cells.
Anthrax edema toxin inhibits Nox1-mediated formation of reactive oxygen species by colon epithelial cells.
复制标题
炭疽水肿毒素抑制 Nox1 介导的结肠上皮细胞活性氧的形成。
DOI：
10.1159/000151481
复制
发表时间：
2009
影响因子：
5.3
通讯作者：
Bokoch,GaryM
中科院分区：
文献类型：
--
作者：
Kim,Jun-Sub;Bokoch,GaryM
炭疽芽孢杆菌（炭疽）孢子中毒的一个主要途径是通过它们的摄入和随后被肠上皮吸收。炭疽水肿毒素（ETx）是一种腺苷酸环化酶，可引起中毒细胞中cAMP的持续升高。NADPH氧化酶（Nox1 - nox5， Duox1和2）产生活性氧（ROS）作为宿主对细菌的先天免疫反应的组成部分，包括胃肠道上皮组织中的Nox1。我们发现ETx能有效抑制HT-29结肠上皮细胞中Nox1形成ROS。这种抑制需要pka介导的nox1调控成分NoxA1的磷酸化，以及随后的14-3-3ζ结合。抑制nox1介导的肠道上皮ROS形成可能是b使用的一种机制。炭疽菌绕过先天免疫反应。
One major route of intoxication byBacillus anthracis(anthrax) spores is via their ingestion and subsequent uptake by the intestinal epithelium. Anthrax edema toxin (ETx) is an adenylate cyclase that causes persistent elevation of cAMP in intoxicated cells. NADPH oxidase enzymes (Nox1–Nox5, Duox1 and 2) generate reactive oxygen species (ROS) as components of the host innate immune response to bacteria, including Nox1 in gastrointestinal epithelial tissues. We show that ETx effectively inhibits ROS formation by Nox1 in HT-29 colon epithelial cells. This inhibition requires the PKA-mediated phosphorylation of the Nox1-regulatory component, NoxA1, and the subsequent binding of 14-3-3ζ. Inhibition of Nox1-mediated ROS formation in the gut epithelium may be a mechanism used byB. anthracisto circumvent the innate immune response.