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首页> 外文期刊>Infection and immunity >Cholera enterotoxin-induced mucus secretion and increase in the mucus blanket of the rabbit ileum in vivo.
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Cholera enterotoxin-induced mucus secretion and increase in the mucus blanket of the rabbit ileum in vivo.

机译：霍乱肠毒素诱导的粘液分泌和体内回肠粘液层的增加。

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The in vivo rabbit ileum was used to study the relationship of cholera enterotoxin-induced water and electrolyte secretion and mucus secretion and to determine whether the enterotoxin influenced the intestinal mucus blanket. In experiments in which luminal fluid viscosity was used to assess mucus secretion, it was found that while cholera enterotoxin induced a sustained secretion of water and electrolytes, the toxin-induced mucus hypersecretion was short lived (3 to 5 h) and subsequent exposure of the mucosa to cholera enterotoxin or prostaglandin E1 did not stimulate mucus secretion further. Dibutyryl cyclic AMP and theophylline caused a modest mucus secretion in ileal loops which differed from that of cholera enterotoxin in both magnitude and in the fact that the mucus secretion occurred 2 to 3 h after the onset of water and electrolyte secretion. An oral replacement solution was used in the ileum to reduce the enterotoxin-induced loss of water and electrolytes into the lumen. While such a solution slowed the appearance of acidic glycoprotein in the intestinal lumen, it did not change the amount of glycoprotein secreted over a 7-h period, suggesting that toxin-induced mucus secretion was not simply due to a flushing action of the experimentally caused diarrhea. To assess mucus blanket thickness, neutral glycoprotein was recovered from the blanket of rabbit ileal loops 7 h after exposure to cholera enterotoxin and the thickness of the mucus blanket was measured directly 4 and 18 h after toxin exposure. Both methods indicated that even though cholera enterotoxin-induced mucus hypersecretion had subsided and there was histological evidence of goblet cell mucin depletion, there was a sustained increase in mucus blanket thickness that was detectable for at least 18 h after mucosal enterotoxin exposure.
机译：体内兔回肠用于研究霍乱肠毒素诱导的水和电解质分泌与粘液分泌的关系，并确定肠毒素是否影响肠粘膜覆盖。在使用腔液粘度评估粘液分泌的实验中，发现虽然霍乱肠毒素诱导了水和电解质的持续分泌，但是毒素诱导的粘液过度分泌是短暂的（3至5小时），随后暴露于粘膜对霍乱肠毒素或前列腺素E1不会进一步刺激粘液分泌。二丁酰环AMP和茶碱在回肠loop中引起适度的粘液分泌，其大小和霍乱肠毒素的分泌均不同，并且在水和电解质分泌开始后2至3 h发生粘液分泌。在回肠中使用口服替代溶液以减少肠毒素引起的水和电解质向内腔的流失。尽管这种溶液减慢了肠腔中酸性糖蛋白的出现，但它并没有改变7小时内分泌的糖蛋白的量，这表明毒素诱导的粘液分泌不仅是由于实验引起的潮红作用引起的。腹泻。为了评估粘液覆盖层的厚度，在暴露于霍乱肠毒素后7 h从兔回肠loop的覆盖层中回收中性糖蛋白，并在暴露毒素后4和18 h直接测量粘液覆盖层的厚度。两种方法均表明，即使霍乱肠毒素引起的粘液分泌过多已消退，并且有组织学证据表明杯状细胞粘蛋白耗竭，但粘膜肠毒素暴露后至少18 h粘液覆盖层厚度持续增加。

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