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Comparison of the Action of Escherichia coli Enterotoxin on the Thymocyte Adenylate Cyclase-Cyclic Adenosine Monophosphate System to That of Cholera Toxin and Prostaglandin E1

机译:大肠杆菌肠毒素对胸腺细胞腺苷酸环化酶-环腺苷一磷酸系统与霍乱毒素和前列腺素E1的作用比较

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Mouse thymocytes were used to compare mechanisms by which Vibrio cholerae and heat-labile Escherichia coli enterotoxins activate the adenylate cyclase-cyclic adenosine monophosphate (AMP) system. Both enterotoxins had their time-delayed increase in cyclic AMP neutralized by antisera to V. cholerae or E. coli enterotoxin, blocked by low concentrations of ganglioside GM1, and destroyed by prior heating. Enterotoxin activation of adenylate cyclase was similarly affected. By contrast, prostaglandin E1-mediated increases in cyclic AMP were not affected by specific antitoxins or gangliosides. Combination of maximal stimulatory doses of both enterotoxins did not produce additive increases in cyclic AMP. Wash experiments suggested that both enterotoxins bind rapidly and tightly to thymocytes at 37 C. However, lowering the incubation temperature to 8 C reduced the affinity of E. coli enterotoxin but not cholera toxin for thymocytes. Results suggest that heat-labile E. coli enterotoxin and cholera enterotoxin may activate the same adenylate cyclase enzyme by similar mechanisms.
机译:小鼠胸腺细胞用于比较霍乱弧菌和热不稳定的大肠杆菌肠毒素激活腺苷酸环化酶-环磷酸腺苷(AMP)系统的机制。两种肠毒素都被抗血清中和至 V中和。霍乱 E。大肠神经毒素,被低浓度的神经节苷脂G M1 阻断,并被事先加热破坏。腺苷酸环化酶的肠毒素激活同样受到影响。相比之下,前列腺素E 1 介导的环AMP的增加不受特定抗毒素或神经节苷脂的影响。两种肠毒素的最大刺激剂量的组合不会在循环AMP中产生加性增加。洗涤实验表明,两种肠毒素均在37°C时与胸腺细胞快速紧密结合。但是,将孵育温度降低至8°C会降低 E的亲和力。大肠杆菌的肠毒素而不是胸腺细胞的霍乱毒素。结果表明,热不稳定的 E。大肠杆菌肠毒素和霍乱肠毒素可能通过相似的机制激活相同的腺苷酸环化酶。

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