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Am J Physiol Gastrointest Liver Physiol 276: G485-G490, 1999;
0193-1857/99 $5.00
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Vol. 276, Issue 2, G485-G490, February 1999

Participation of reactive oxygen metabolites in Clostridium difficile toxin A-induced enteritis in rats

Bosheng Qiu1, Charalabos Pothoulakis1, Ignazio Castagliuolo1, Sigfus Nikulasson2, and J. Thomas LaMont1

1 Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston 02215; and 2 Mallory Institute, Department of Pathology, Boston University Medical Center Hospital, Boston, Massachusetts 02118

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 of Clostridium 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 of C. difficile toxin 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.

superoxide radicals; hydroxyl radicals; intestinal inflammation; intestinal secretion; enterotoxins


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