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ICAM‐1‐dependent pathways regulate colonic eosinophilic inflammation
Author(s) -
Forbes Elizabeth,
Hulett Mark,
Ahrens Richard,
Wagner Norbert,
Smart Vanessa,
Matthaei Klaus I.,
Brandt Eric B.,
Dent Lindsay A.,
Rothenberg Marc E.,
Tang Mimi,
Foster Paul. S.,
Hogan Simon P.
Publication year - 2006
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1105643
Subject(s) - eosinophil , addressin , biology , cell adhesion molecule , inflammation , integrin , immunology , intercellular adhesion molecule , cell adhesion , intercellular adhesion molecule 1 , microbiology and biotechnology , receptor , cell , biochemistry , asthma
Eosinophilic inflammation is a common feature of numerous eosinophil‐associated gastrointestinal (EGID) diseases. Central to eosinophil migration into the gastrointestinal 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 β 7 ‐integrin addressin cell adhesion molecule‐1‐independent pathway. Characterization of integrin expression on colonic eosinophils by flow cytometry analysis revealed that colonic CC chemokine receptor 3 + eosinophils express the intercellular adhesion molecule‐1 (ICAM‐1) counter‐receptor integrins α L , α M , and β 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 β 2 ‐integrin/ICAM‐1‐dependent pathways are integral to eosinophil recruitment into the colon during GI inflammation associated with colonic injury.