Role of the W07-toxin on Vibrio cholerae-induced diarrhoea

Role of the W07-toxin on Vibrio cholerae-induced diarrhoea
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DOI:
10.1016/j.bbagen.2003.10.016
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发表时间:
2004-01-05
影响因子:
3
通讯作者:
Majumdar, S
Majumdar, S
中科院分区:
生物学3区
文献类型:
--
作者:
Bhattacharyya, S;Ghosh, S;Majumdar, S

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从印度南部霍乱疫情中分离到的霍乱纤维菌W07株缺乏CTX基因,但仍能分泌一种新的毒素--W07-毒素,该毒素可导致结扎的兔回肠回肠积液。本研究涉及的重要细胞内信使有钙离子、环磷酸腺苷、三磷酸肌醇和蛋白激酶C。一些抑制剂/通道阻滞剂进一步显示了[Ca~(2+)](I)在毒素诱导的细胞反应中的主要调节作用。W07毒素刺激的肠上皮细胞内ROS水平的升高与抗氧化酶、过氧化氢酶和超氧化物歧化酶(SOD)水平的降低有关。通过测定亚硝酸盐和瓜氨酸水平检测到的活性氮中间产物(RNI)在W07毒素触发的肠上皮细胞中含量很高,从而表明它们在毒素介导的粘膜通透性变化中所起的作用。W07毒素与免疫球蛋白(WT)(从抗毒素血清中分离出的免疫球蛋白)或GM(1)一起预先孵育的实验也证实了毒素的确切作用。因此,第二信使水平的显著增加和抗氧化防御能力的降低似乎在介导这种新的霍乱毒素引起的液体分泌方面起着重要作用。(C)2003年,爱思唯尔出版。
Fibrio cholerae W07 strain isolated from a cholera epidemic in South India, lacked the ctx gene but could still secrete a novel toxin, the W07-toxin that could cause fluid accumulation in ligated rabbit ileal loop. The important intracellular messengers implicated in this study were Ca2+, cyclic AMP, inositol triphosphate and protein kinase C (PKC). A number of inhibitors/channel blockers have further shown the major role of [Ca2+](i) in modulation of the toxin-induced cellular response. An increase in the level of reactive oxygen species (ROS) in the W07-toxin-stimulated enterocytes correlated with the decrease in the levels of antioxidant enzymes, catalase and superoxide dismutase (SOD). The reactive nitrogen intermediates (RNI) detected by measuring the levels of nitrite and citrulline, were found to be high in the enterocytes triggered with the W07-toxin, thereby indicating their role in toxin-mediated change in mucosal permeability. The precise role of the toxin has also been authenticated by conducting the experiments with W07-toxin preincubated in the presence of IgG(WT) (IgG isolated from antitoxin sera) or GM(1). Thus, a significant increase in the levels of second messengers and a decrease in antioxidant defenses appear to be important in mediating the fluid secretion caused by this novel toxin from V cholerae W07. (C) 2003 Published by Elsevier B.V.