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American Journal of Respiratory and Critical Care Medicine Vol 167. pp. 164-170, (2003)
© 2003 American Thoracic Society

Original Article

Platelet Endothelial Cell Adhesion Molecule-1 in Neutrophil Emigration during Acute Bacterial Pneumonia in Mice and Rats

Sadatomo Tasaka, Lan Qin, Ariko Saijo, Steven M. Albelda, Horace M. DeLisser and Claire M. Doerschuk

Department of Pediatrics, Rainbow Babies and Children's Hospital, Case Western Reserve University, Cleveland, Ohio; Physiology Program, Harvard School of Public Health, Boston, Massachusetts; Herman B. Wells Center for Pediatric Research and the Section of Pulmonology and Intensive Care, the Departments of Pediatrics and Anatomy, Indiana University, Indianapolis, Indiana; and Pulmonary Allergy and Critical Care Division, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

Correspondence and requests for reprints should be addressed to Claire M. Doerschuk, M.D., Rainbow Babies and Children's Hospital, Room 787, 11100 Euclid Avenue, Cleveland, OH 44106. E-mail: cmd22{at}po.cwru.edu

Platelet endothelial cell adhesion molecule-1 (PECAM-1) (CD31) is an adhesion molecule believed to mediate transendothelial migration of neutrophils and other leukocytes after CD11/CD18-mediated adhesion. Our study evaluated the role of PECAM-1 in neutrophil emigration across the pulmonary capillaries and the bronchial microvasculature using blocking anti–PECAM-1 antibodies in mice and rats. Neutrophil emigration was induced by Escherichia coli, a stimulus eliciting CD11/CD18-dependent emigration, or Streptococcus pneumoniae, a stimulus inducing CD11/CD18-independent emigration. Although anti–PECAM-1 antibodies partially inhibited glycogen-induced neutrophil emigration into the peritoneum, neutrophil emigration across either the pulmonary capillaries or the bronchial microvasculature in response to either E. coli or S. pneumoniae was not prevented when the function of PECAM-1 was inhibited in either mice or rats. There was also no increase in the number of intravascular neutrophils within the bronchial vessels after treatment with anti–PECAM-1 antibody. These studies indicate that either CD11/CD18-dependent or -independent adhesion pathways may lead to PECAM-1–independent transendothelial migration through the pulmonary or the bronchial endothelium.

Key Words: rodent • lung • neutrophils • infectious immunity-bacteria • adhesion molecules




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