Microflora-derived polyamines modulate obstruction-induced colonic mucosal hypertrophy.

Microflora-derived polyamines modulate obstruction-induced colonic mucosal hypertrophy.
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微生物群衍生的多胺可调节阻塞引起的结肠粘膜肥大。

DOI:
10.1152/ajpgi.1989.256.6.g1049
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发表时间:
1989
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Seidel,ER
Seidel,ER
中科院分区:
--
文献类型:
--
作者:
Osborne,DL;Seidel,ER

文献摘要

被引文献

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本实验旨在确定微生物区系来源的肠腔内多胺在结肠粘膜对梗阻的反应中的作用。Sprague-Dawley大鼠经口给予0.9%NaCl或不可吸收抗生素的组合,然后放置假或完全结肠梗阻。手术后66小时,NaCl处理动物梗阻近端粘膜的湿组织重量、DNA、RNA和蛋白质含量均增加;然而,DNA含量是抗生素治疗后唯一增加的参数。这种诱导是一种纯粹的局部效应,因为在梗阻远端的回肠或结肠中未观察到增生或肥大。在NaCl处理的动物中,粘膜鸟氨酸脱羧酶活性直到术后48小时才被诱导,但粘膜亚精胺浓度早在24小时就显著升高。肠腔内细菌赖氨酸,鸟氨酸,精氨酸脱羧酶活性诱导梗阻,但减少抗生素治疗。本研究中使用的抗生素阻断了培养中肠上皮细胞(IEC-6)对[14 C]腐胺的摄取,但[14 C]-赖氨酸转运相对不受影响。这些数据表明,肠腔内多胺调节肠梗阻后结肠粘膜的营养反应。
Experiments were designed to determine the role of microflora-derived intraluminal polyamines in the colonic mucosal response to obstruction. Sprague-Dawley rats were treated per os with 0.9% NaCl or a combination of nonabsorbable antibiotics prior to the placement of either a sham or complete colonic obstruction. Sixty-six hours after surgery, wet tissue weight, DNA, RNA, and protein content were all increased in the mucosa proximal to the obstruction in NaCl-treated animals; however, DNA content was the only parameter increased after antibiotics. This induction was a purely local effect as neither hyperplasia nor hypertrophy was observed in the ileum or colon distal to the obstruction. In the NaCl-treated animals, mucosal ornithine decarboxylase activity was not induced until 48 h postsurgery, yet mucosal spermidine concentrations were significantly higher as early as 24 h. Intraluminal bacterial lysine, ornithine, and arginine decarboxylase activities were induced by obstruction but were reduced by antibiotic treatment. [14C]putrescine uptake by intestinal epithelial cells (IEC-6) in culture was blocked by the antibiotics employed in this study, but [14C]-lysine transport was relatively unaffected. These data demonstrate that intraluminal polyamines modulate the trophic response of the colonic mucosa after colonic obstruction.