Escherichia coli enterotoxin (STa) binds to receptors, stimulates guanyl cyclase, and impairs absorption in rat colon.

Escherichia coli enterotoxin (STa) binds to receptors, stimulates guanyl cyclase, and impairs absorption in rat colon.
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大肠杆菌肠毒素 (STa) 与受体结合,刺激鸟苷酸环化酶,并损害大鼠结肠的吸收。

DOI:
10.1016/0016-5085(92)90163-s
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发表时间:
1992
期刊:
影响因子:
29.4
通讯作者:
Cohen,MB
Cohen,MB
中科院分区:
医学1区
文献类型:
--
作者:
Mezoff,AG;Giannella,RA;Eade,MN;Cohen,MB

文献摘要

被引文献

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为了确定大肠杆菌热稳定肠毒素介导的结肠炎中结肠的作用,比较了大鼠结肠和回肠中的毒素结合、鸟苷酸环化酶激活和毒素诱导的水通量。Scatchard分析表明,在结肠细胞和回肠细胞中均存在一类热稳定的肠毒素受体,其亲和力常数均为109 L/mol,但在结肠细胞中每个细胞的毒素受体数量是回肠细胞的3.5倍(8.32 ± 1.33 × 105 vs. 2.33± 0.28 × 105个受体/细胞;P= 0.02)。热稳定性肠毒素刺激鸟苷酸环化酶激活在近端结肠和回肠膜以相同的剂量依赖性方式,具有相似的敏感性和最大响应。在8 nmol/L的剂量下,热稳定性肠毒素对结肠和回肠的净水通量也有相似的抑制程度(分别为−47.8和−48.4 μL · cm−1· h−1)。在结肠中的该剂量下,由于吸收基线较高,吸收继续,但水平降低。在回肠中的该剂量下,热稳定性肠毒素诱导净分泌。这些数据与热稳定性肠毒素诱导的结肠炎是由于小肠液分泌增加导致结肠吸收能力下降的概念一致。
To determine the contribution of the colon inEscherichia coliheat-stable enterotoxin-mediated diarrheal disease, toxin binding, guanyl cyclase activation, and toxin-induced water flux in the rat colon and ileum were compared. Scatchard analysis suggested a single class of heat-stable enterotoxin receptors with an affinity constant of binding of 109L/mol in both colonocytes and ileocytes; however, the number of toxin receptors per cell was 3.5-fold greater in colonocytes than ileocytes (8.32 ± 1.33 × 105vs. 2.33 ± 0.28 × 105receptors per cell;P= 0.02). Heat-stable enterotoxin stimulated guanyl cyclase activation in an identical dose-dependent manner in proximal colonic and ileal membranes, with similar sensitivity and maximum response. Heat-stable enterotoxin also inhibited net water flux to a similar degree in both colon and ileum (−47.8 vs. −48.4 μL · cm−1· h−1, respectively) at a dose of 8 nmol/L. At this dose in the colon, because of a higher baseline of absorption, absorption continued, but at a diminished level. At this dose in the ileum, heat-stable enterotoxin induced net secretion. These data are consistent with the concept that heat-stable enterotoxin-induced diarrheal disease results from a decreased absorptive capacity in the colon in the face of increased small intestinal fluid secretion.