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Am J Physiol Lung Cell Mol Physiol 283: L180-L187, 2002. First published February 22, 2002; doi:10.1152/ajplung.00430.2001
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Vol. 283, Issue 1, L180-L187, July 2002

ICAM-1 facilitates alveolar macrophage phagocytic activity through effects on migration over the AEC surface

Robert Paine III, Susan B. Morris, Hong Jin, Carlos E. O. Baleeiro, and Steven E. Wilcoxen

Division of Pulmonary and Critical Care Medicine, Department of Veterans Affairs Medical Center, University of Michigan, Ann Arbor, Michigan 48105

We postulate that intercellular adhesion molecule-1 (ICAM-1) on type I alveolar epithelial cells (AEC) facilitates phagocytic activity of alveolar macrophages (AM) in the alveolus. When wild-type and ICAM-1-deficient mice were inoculated intratracheally with FITC-labeled microspheres, AM phagocytosis of beads (after 1 and 4 h) was significantly reduced in ICAM-1-/- mice compared with controls. To focus on ICAM-1-mediated interactions specifically involving AM and AEC, rat AM were placed in culture with rat AEC treated with neutralizing anti-ICAM-1 F(ab')2 fragments. Blocking ICAM-1 significantly decreased the AM phagocytosis of beads. Planar chemotaxis of AM over the surface of AEC was also significantly impaired by neutralization of AEC ICAM-1. ICAM-1 in rat AEC is associated with the actin cytoskeleton. Planar chemotaxis of AM was also significantly reduced by pretreatment of the AEC monolayer with cytochalasin B to disrupt the actin cytoskeleton. These studies indicate that ICAM-1 on the AEC surface promotes mobility of AM in the alveolus and is critically important for the efficient phagocytosis of particulates by AM.

pulmonary alveoli; inflammation; host defense; lung; intercellular adhesion molecule-1; alveolar epithelial cells


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