The Journal of Experimental Medicine
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Published online 1 January 2001.
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© The Rockefeller University Press, 0022-1007/2001/1/25/ $5.00
The Journal of Experimental Medicine, Volume 193, Number 1, January 1, 2001 25-34

Original Article

Role of the High Affinity Immunoglobulin E Receptor in Bacterial Translocation and Intestinal Inflammation

David Dombrowicza, Sophie Nuttenc, Pierre Desreumauxc, Christel Neutd, Gérard Torpierb, Marc Peeterse, Jean-Frédéric Colombelc, and Monique Caprona

a Institut National de la Sante et de la Recherche Medicale U167, Institut Pasteur de Lille, 59019 Lille, France
b Institut National de la Sante et de la Recherche Medicale U325, Institut Pasteur de Lille, 59019 Lille, France
c Laboratoire de Recherche sur les Maladies Inflammatoires Intestinales et Département d'Hépatogastroenterologie, Centre Hospitalier Régional Universitaire de Lille, 59045 Lille, France
d Faculty of Pharmacy, University of Lille II, 59045 Lille, France
e Department of Gastroenterology, University Hospital Gasthuisberg, B-3000 Leuven, Belgium
INSERM U167, Institut Pasteur de Lille, 1 rue Professeur Calmette, BP245, 59019 Lille Cedex, France.33-320-87-78-8833-320-87-79-62

monique.capron{at}pasteur-lille.fr

A role for immunoglobulin E and its high affinity receptor (Fc{varepsilon}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{varepsilon}RI (hFc{varepsilon}RI), with a cell distribution similar to that in humans, to Fc{varepsilon}RI-deficient animals. In hFc{varepsilon}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{varepsilon}RI transgenic mice, 2,4,6-tri-nitrobenzenesulfonic acid (TNBS)-induced colitis was also more pronounced, whereas Fc{varepsilon}RI-deficient animals were protected from colitis, demonstrating that Fc{varepsilon}RI can affect the onset of intestinal inflammation.

Key Words: immunoglobulin E receptor • bacterial translocation • intestinal permeability • inflammatory bowel disease • colitis

D. Dombrowicz, S. Nutten, and P. Desreumaux contributed equally to this work.

Abbreviations used in this paper: CD, Crohn's disease; hFc{varepsilon}RI, human Fc{varepsilon}RI; IBD, inflammatory bowel disease, MLN, mesenteric lymph node, RT, reverse transcription; SPF, specific pathogen-free; Tg, transgenic; TNBS, 2,4,6-tri-nitrobenzenesulfonic acid; WT, wild-type.

© 2001 The Rockefeller University Press


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