|
||
Original Article |
Correspondence to: Monique Capron, INSERM U167, Institut Pasteur de Lille, 1 rue Professeur Calmette, BP245, 59019 Lille Cedex, France. Tel:33-320-87-79-62 Fax:33-320-87-78-88 E-mail:monique.capron{at}pasteur-lille.fr.
A role for immunoglobulin E and its high affinity receptor (Fc
RI) in the control of bacterial pathogenicity and intestinal inflammation has been suggested, but relevant animal models are lacking. Here we compare transgenic mice expressing a humanized Fc
RI (hFc
RI), with a cell distribution similar to that in humans, to Fc
RI-deficient animals. In hFc
RI transgenic mice, levels of colonic interleukin 4 were higher, the composition of fecal flora was greatly modified, and bacterial translocation towards mesenteric lymph nodes was increased. In hFc
RI transgenic mice, 2,4,6-tri-nitrobenzenesulfonic acid (TNBS)-induced colitis was also more pronounced, whereas Fc
RI-deficient animals were protected from colitis, demonstrating that Fc
RI can affect the onset of intestinal inflammation.
Key Words: immunoglobulin E receptor, bacterial translocation, intestinal permeability, inflammatory bowel disease, colitis
| TABLE OF CONTENTS |
|