Participation of reactive oxygen metabolites in Clostridium difficile toxin A-induced enteritis in rats.
Participation of reactive oxygen metabolites in Clostridium difficile toxin A-induced enteritis in rats.
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活性氧代谢物参与艰难梭菌毒素 A 诱导的大鼠肠炎。
DOI：
10.1152/ajpgi.1999.276.2.g485
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
LaMont,JT
中科院分区：
文献类型：
--
作者：
Qiu,B;Pothoulakis,C;Castagliuolo,I;Nikulasson,S;LaMont,JT
活性氧代谢物（ROM）有助于肠道炎症的病理生理学。我们的目的是确定 ROM 与艰难梭菌毒素 A 产生的大鼠实验性回肠炎的关系。管腔内毒素 A 导致回肠微粒体产生的羟自由基和过氧化氢显着增加，在毒素暴露后 1 小时开始，并在 2-3 小时达到峰值，而这种情况可以通过用 DMSO（一种 ROM 清除剂）或超氧化物歧化酶 (SOD) 预处理来抑制，超氧化物歧化酶 (SOD) 会灭活 ROM。相比之下，接触毒素A后，粘膜黄嘌呤氧化酶仅略有增加，而黄嘌呤氧化酶抑制剂别嘌呤醇对毒素A相关的肠道反应没有影响。中性粒细胞减少症的诱导导致毒素介导的自由基形成、液体分泌和渗透性减少。 C.肠毒性作用艰难梭菌毒素 A 与回肠组织中 ROM 释放增加有关，而 ROM 抑制剂 DMSO 和 SOD 可以抑制这些作用。这表明，A 毒素肠炎期间释放的 ROM 主要是由侵入发炎肠段的中性粒细胞释放的。
Reactive oxygen metabolites (ROMs) contribute to the pathophysiology of intestinal inflammation. Our aim was to ascertain the involvement of ROMs in experimental ileitis in rats produced by toxin A ofClostridium difficile. Intraluminal toxin A caused a significant increase in hydroxyl radical and hydrogen peroxide production by ileal microsomes starting 1 h following toxin exposure and peaking at 2–3 h, and this was inhibited by pretreatment with DMSO, a ROM scavenger, or superoxide dismutase (SOD), which inactivates ROMs. In contrast, mucosal xanthine oxidase increased only slightly after toxin A exposure, and allopurinol, an inhibitor of xanthine oxidase, had no effect on toxin A-associated intestinal responses. Induction of neutropenia resulted in reduction of toxin-mediated free radical formation, fluid secretion, and permeability. The enterotoxic effects ofC. difficiletoxin A were associated with increased ROM release in ileal tissues, and the ROM inhibitors DMSO and SOD inhibited these effects. This suggests that ROMs released during toxin A enteritis are released primarily from neutrophils invading the inflamed bowel segment.