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Intercellular Adhesion Molecule-1 Plays a Pivotal Role in Endotoxin-Induced Airway Disease*

David M. Brass, PhD; Jordan D. Savov, MD, PhD; David A. Schwartz, MD, MPH, FCCP
Author and Funding Information

*From the Department of Pulmonary and Critical Care Medicine, Duke University Medical Center, Durham, NC.

Correspondence to: David A. Schwartz, MD, MPH, FCCP, DUMC 2629, Room 275 MSRB, Research Drive, Durham, NC 27710; e-mail: david.Schwartz@duke.edu



Chest. 2003;123(3_suppl):416S. doi:10.1378/chest.123.3_suppl.416S
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Extract

Airway inflammation and airway hyperresponsiveness (AHR) are fundamental features of asthma. Migration of inflammatory cells from the circulation into the airways is mediated in part by adhesion molecules such as intercellular adhesion molecule (ICAM)-1, which are expressed on vascular endothelial cells, and the β2 integrin CD11b/CD18, which is expressed on neutrophils. Increasing evidence suggests that ICAM-1 and CD11b/CD18 also have signaling capabilities, suggesting that they might modulate airway reactivity independently of their adhesion properties.

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