首页> 外文期刊>Infection and immunity >Lanthanum inhibition of Vibrio cholerae and Escherichia coli enterotoxin-induced enterosorption and its effects on intestinal mucosa cyclic adenosine 3',5'-monophosphate and cyclic guanosine 3',5'-monophosphate levels.
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Lanthanum inhibition of Vibrio cholerae and Escherichia coli enterotoxin-induced enterosorption and its effects on intestinal mucosa cyclic adenosine 3',5'-monophosphate and cyclic guanosine 3',5'-monophosphate levels.

机译:镧抑制弧菌霍乱和大肠杆菌肠毒素诱导的肠溶毒素及其对肠粘膜环状腺苷3',5'-单磷酸盐和环状鸟嘌呤3',5'-一磷酸盐水平的影响。

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Several trivalent cations, including lanthanum (La3+), inhibited the secretion (enterosorption) induced by the enterotoxins of Vibrio cholerae and Escherichia coli in the rabbit ileum in vivo. High concentrations (greater than 10 mM) of La3+ were required to inhibit cholera enterotoxin (CE)-induced enterosorption, probably because of the adsorption of the La3+ often potentiated the CE-induced enterosorption. If luminal La3+ exposure followed CE exposure, some recovery of the enterosorptive response was observed. The longer the lag between the CE exposure and the La3+ exposure, the greater was the recovery of the enterosorptive response. Lanthanum inhibited HCO3- secretion more than Cl- secretion. By altering the luminal fluid pH at the time of La3+ exposure, it was found that La3+ was adsorbed to negatively charged luminal sites, having an apparent pK between 2.5 and 3.0. Although La3+ antagonized the enterosorptive response to CE, it mimicked rather than antagonized the cyclic adenosine 3',5'-monophosphate elevation and cyclic guanosine 3',5'-monophosphate depression induced by the toxin. It is therefore concluded that the La3+ inhibition of the CE-induced enterosorption must have occurred at a site following the generation of the cyclic nucleotides. Cholera enterotoxin caused complex time-dependent changes in the mucosal cyclic adenosine 3',5'-monophosphate and cyclic guanosine 3',5'-monophosphate levels, as revealed by studying tissue cyclic adenosine 3',5'-monophosphate/cyclic guanosine 3',5'-monophosphate ratios. The possible roles these two cyclic nucleotides may play in the pathogenesis of the cholera diarrhea are discussed.
机译:几个三价阳离子,包括镧(La3 +),抑制了在体内兔回肠中肠胆碱基和大肠杆菌的肠毒素诱导的分泌(肠溶)。需要高浓度(大于10 mm)的La3 +来抑制霍乱肠毒素(Ce)诱导肠溶剂,可能是因为La3 +的吸附+常有增强的Ce诱导的肠溶剂。如果腔拉3 +曝光遵循Ce暴露,则观察到肠溶反应的一些回收。 Ce暴露和La3 +暴露之间的滞后越长,肠溶反应的恢复越大。镧抑制了HCO3-分泌物比Cl-分泌更高。通过改变La3 +暴露时的腔流体pH,发现La3 +被吸附到带负电的腔位置,表观PK在2.5和3.0之间。虽然La3 +对Ce的肠溶反应拮抗,但它模仿而不是拮抗毒素诱导的循环腺苷3',5'-单磷酸升高和循环鸟嘌呤3',5'-单磷酸盐抑郁症。因此,得出结论,La3 +抑制Ce诱导的肠溶吸收的抑制必须在产生环核苷酸后的部位发生。霍乱肠毒素引起粘膜环状腺苷3',5'-单磷酸盐和环状鸟嘌呤3',5'-一磷酸含量的复杂时间依赖性变化,如通过研究组织环状腺苷3',5'-单磷酸/环状鸟嘌呤3所揭示的',5'-单磷酸盐比率。讨论了可能在霍乱腹泻的发病机制中发挥这两个环状核苷酸的可能作用。

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