Published online before print February 28, 2002, doi: 10.1161/01.RES.0000013835.53611.97
© 2002 American Heart Association, Inc.
Cellular Biology |
Role of 
4 Integrin and VCAM-1 in CD18-Independent Neutrophil Migration Across Mouse Cardiac Endothelium
From the Department of Immunology (R.A.B.),Walter Reed Army Institute of Research, Silver Spring, Md; DeBakey Heart Center at Baylor College of Medicine and Methodist Hospital (Z.-M.D., E.M.D., L.H.M., C.M.B., A.R.B.), Houston, Tex; and the Department of Clinical Studies (T.K.P.), Central Laboratory, Royal Veterinary and Agricultural University, Copenhagen, Denmark.
Correspondence to Alan R. Burns, Depts of Medicine and Pediatrics, Sections of Cardiovascular Sciences and Leukocyte Biology, Baylor College of Medicine, Room 515B, One Baylor Plaza, Houston, TX 77030. E-mail aburns{at}bcm.tmc.edu
Myocardial damage due to reperfusion of ischemic tissue is caused primarily by infiltrating neutrophils. Although leukocyte ß2 integrins (CD18) play a critical role, significant neutrophil emigration persists when CD18 is neutralized or absent. This study examined the role of leukocyte ß1 integrin (
4) and its endothelial ligand VCAM-1 in CD18-independent neutrophil migration across cardiac endothelium. In a mouse model of myocardial ischemia and reperfusion, we show that compared with wild-type mice, neutrophil infiltration efficiency was reduced by 50% in CD18-null mice; in both types of mice, myocardial VCAM-1 staining increased after reperfusion. In wild-type mice, antibodies against CD18, ICAM-1 (an endothelial ligand for CD18), or VCAM-1 given 30 minutes before ischemia did not block neutrophil emigration at 3 hours reperfusion. Although anti-VCAM-1 attenuated neutrophil emigration by 90% in CD18-null mice, it did not diminish myocardial injury. To determine if CD18-independent neutrophil emigration was a tissue-specific response, we used isolated peripheral blood neutrophils from wild-type or CD18-null mice and showed neutrophil migration across lipopolysaccharide-activated cultured cardiac endothelium is CD18-independent, whereas migration across endothelium obtained from inferior vena cava is CD18-dependent. Consistent with our in vivo findings, migration of CD18-deficient neutrophils on cardiac endothelial monolayers is blocked by antibodies against 4 integrin or VCAM-1. We conclude tissue-specific differences in endothelial cells account, at least partially, for CD18-independent neutrophil infiltration in the heart.
Key Words: neutrophil • myocardium • reperfusion • vascular cell adhesion molecule-1 • 4 integrin
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