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Gastroenterology. 1998 May;114(5):956-64.

Direct evidence of mast cell involvement in Clostridium difficile toxin A-induced enteritis in mice.

Author information

1
Combined Program in Pediatric Gastroenterology and Nutrition, Children's Hospital and Massachusetts General Hospital, Boston, Massachusetts, USA. bwershil@bidmc.harvard.edu

Abstract

BACKGROUND & AIMS:

The pathogenesis of Clostridium difficile toxin A-induced intestinal inflammation is not completely understood. The aim of this study was to define the contribution of mast cells to the fluid secretion and neutrophil infiltration associated with toxin A-induced enteritis.

METHODS:

Fluid secretion and neutrophil infiltration in toxin A- or buffer-challenged ileal loops were assessed in normal, mast cell-deficient, and mast cell-deficient KitW/KitW-v mice that had undergone selective repair of their mast cell deficiency. The effect of a specific substance P-receptor antagonist was also studied.

RESULTS:

Intestinal fluid secretion and neutrophil recruitment were significantly diminished in mast cell-deficient KitW/KitW-v and mast cell-deficient MgfSl/MgfSl-d mice compared with the respective normal mice. Mast cell-reconstituted KitW/KitW-v mice showed responses similar to the normal congenic mice. Administration of a specific substance P-receptor antagonist (CP-96,345) reduced toxin A-induced intestinal fluid secretion and inhibited neutrophil infiltration in normal, mast cell-deficient KitW/KitW-v, and mast cell-reconstituted KitW/KitW-v mice.

CONCLUSIONS:

C. difficile toxin A elicits intestinal fluid secretion and neutrophil infiltration by both mast cell-dependent and -independent pathways, and substance P participates in both pathways.

PMID:
9558284
DOI:
10.1016/s0016-5085(98)70315-4
[Indexed for MEDLINE]

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