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Am J Physiol Gastrointest Liver Physiol 280: G539-G545, 2001;
0193-1857/01 $5.00
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Vol. 280, Issue 4, G539-G545, April 2001

Endogenous corticosteroids modulate Clostridium difficile toxin A-induced enteritis in rats

Ignazio Castagliuolo1, Katia Karalis1,2, Leyla Valenick1, Asiya Pasha1, Sigfus Nikulasson3, Michael Wlk1, and Charalabos Pothoulakis1

1 Division of Gastroenterology, Beth Israel Deaconess Medical Center, and 2 Division of Endocrinology, Children's Hospital, Harvard Medical School, Boston 02215; and 3 Mallory Institute, Department of Pathology, Boston University School of Medicine, Boston, Massachusetts 02218

We examined the role of glucocorticoids in acute inflammatory diarrhea mediated by Clostridium difficile toxin A. Toxin A (5 µg) or buffer was injected in rat ileal loops, and intestinal responses were measured after 30 min to 4 h. Ileal toxin A administration increased plasma glucocorticoids after 1 h, at which time the toxin-stimulated secretion was not significant. Administration of the glucocorticoid analog dexamethasone inhibited toxin A-induced intestinal secretion and inflammation and downregulated toxin A-mediated increase of macrophage inflammatory protein-2. Adrenalectomy followed by replacement with glucocorticoids at various doses suggested that intestinal responses to toxin A were related to circulating levels of glucocorticoids. Administration of the glucocorticoid receptor antagonist RU-486 enhanced toxin A-mediated intestinal secretion and inflammation. We conclude that C. difficile toxin A causes increased secretion of endogenous glucocorticoids, which diminish the intestinal secretory and inflammatory effects of toxin A.

hypothalamic-pituitary adrenal axis; bacterial enterotoxins; macrophage inflammatory protein-2


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