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Am J Physiol Lung Cell Mol Physiol (February 22, 2002). doi:10.1152/ajplung.00430.2001
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Articles in PresS, published online ahead of print February 22, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00430.2001
Submitted on November 2, 2001
Accepted on February 15, 2002

ICAM-1 FACILITATES ALVEOLAR MACROPHAGE PHAGOCYTIC ACTIVITY THROUGH EFFECTS ON MIGRATION OVER THE ALVEOLAR EPITHELIAL CELL SURFACE

Robert Paine1*, Susan B Morris1, Hong Jin1, Carlos E Baleeiro1, and Steven E Wilcoxen1

1 Internal Medicine/Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, Michigan, USA; Pulmonary Section, Department of Veterans Affairs Medical Center, Ann Arbor, Michigan, USA

* To whom correspondence should be addressed. E-mail: rpaine{at}umich.edu.

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 hrs) was significantly reduced in ICAM-1-/- mice compared to controls. To focus on ICAM-1-mediated interactions specifically involving AM and AEC, rat AM were placed in culture with rat AEC that had been 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 also was significantly impaired by neutralization of AEC ICAM-1. ICAM-1 in rat AEC is associated with the actin cytoskeleton. Planar chemotaxis of AM also was significantly reduced by pre-treatment 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.




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