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Published online before print May 26, 2006

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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1105643

Received for publication November 9, 2005.
Revised March 14, 2006.
Accepted for publication March 27, 2006.

Article

ICAM-1-dependent pathways regulate colonic eosinophilic inflammation

Elizabeth Forbes ^*, Mark Hulett , Richard Ahrens , Norbert Wagner , Vanessa Smart ^*, Klaus I. Matthaei ^¶, Eric B. Brandt , Lindsay A. Dent ^||, Marc E. Rothenberg , Mimi Tang ^**, Paul. S. Foster* , and Simon P. Hogan ^@

*Allergy and Inflammation Research Group and ^¶Gene Targeting Group, Division of Biochemistry and Molecular Biology, and Cancer and Vascular Biology Group, Division of Immunology and Genetics, The John Curtin School of Medical Research, Australian National University, Canberra; Asthma, Allergy and Inflammation Research Centre, School of Biomedical Sciences, University of Newcastle, Australia; ^||School of Molecular and Biomedical Science, University of Adelaide, Australia; **Department of Immunology, Murdoch Childrens Research Institute, Royal Children’s Hospital, Victoria, Australia; Department of Pediatrics, City Hospital of Dortmund, Germany; and Division of Allergy and Immunology, Department of Pediatrics, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Ohio

^@ To whom correspondence should be addressed. E-mail: Simon.Hogan{at}cchmc.org.

	Abstract

Eosinophilic inflammation is a common feature of numerous eosinophil-associated gastrointestinal (GI) diseases. Central to eosinophil migration into the GI tract are the integrin-mediated interactions with adhesion molecules. Although the mechanisms regulating eosinophil homing into the small intestine have begun to be elucidated, the adhesion pathways responsible for eosinophil trafficking into the large intestine are unknown. We investigated the role of adhesion pathways in eosinophil recruitment into the large intestine during homeostasis and disease. First, using a hapten-induced colonic injury model, we demonstrate that in contrast to the small intestine, eosinophil recruitment into the colon is regulated by a ₄₇/mucosal addressin cell adhesion molecule-1-independent pathway. Characterization of integrin expression on eosinophils by flow cytometry analysis revealed that colonic CC chemokine receptor 3⁺ eosinophils express the intercellular adhesion molecule-1 (ICAM-1) counter-receptor integrins _L, _M, and ₂. Using ICAM-1-deficient mice and anti-ICAM-1 neutralizing antibodies, we show that hapten-induced colonic eosinophilic inflammation is critically dependent on ICAM-1. These studies demonstrate that ₂-integrin/ICAM-1-dependent pathways are integral to eosinophil recruitment into the colon during GI inflammation associated with colonic injury.

Key Words: eosinophils • adhesion molecules • gastrointestinal tract

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