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

• Published in: American journal of respiratory and critical care medicine Vol. 167; no. 2; pp. 164 - 170
• Main Authors: Tasaka, Sadatomo, Qin, Lan, Saijo, Ariko, Albelda, Steven M, DeLisser, Horace M, Doerschuk, Claire M
• Format: Journal Article
• Language: English
• Published: New York, NY Am Thoracic Soc 15.01.2003; American Lung Association
• Subjects: Acute Disease; Analysis of Variance; Animals; Bacterial diseases; Bacterial diseases of the respiratory system; Biological and medical sciences; CD11 Antigens - metabolism; CD18 Antigens - analysis; CD18 Antigens - metabolism; Chemotaxis, Leukocyte - physiology; Disease Models, Animal; Escherichia coli; Human bacterial diseases; Infectious diseases; Medical sciences; Mice; Mice, Inbred C57BL; Neutrophils; Platelet Endothelial Cell Adhesion Molecule-1 - analysis; Platelet Endothelial Cell Adhesion Molecule-1 - metabolism; Pneumonia, Bacterial - immunology; Pneumonia, Bacterial - microbiology; Pneumonia, Bacterial - physiopathology; Random Allocation; Rats; Rats, Inbred Lew; Rats, Sprague-Dawley; Reference Values; Sensitivity and Specificity; Streptococcus pneumoniae; Pneumonia; Rat; Pathogenesis; Escherichia coli; Migration; Microcirculation; adhesion molecules; Blood vessel; rodent; Bacteria; Micrococcales; neutrophils; Enterobacteriaceae; Lung disease; Pathophysiology; Respiratory disease; Rodentia; Cell adhesion molecule; Bronchus; Streptococcus pneumoniae; Infection; lung; Streptococcaceae; infectious immunity-bacteria; Vertebrata; Mammalia; Mouse; Animal; Bacteriosis; Platelet endothelial cell adhesion molecule 1; Blood capillary; Circulatory system; Neutrophil
• ISSN: 1073-449X; 1535-4970
• DOI: 10.1164/rccm.2202011

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.