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Am J Physiol Lung Cell Mol Physiol 291: L1050-L1058, 2006. First published June 30, 2006; doi:10.1152/ajplung.00067.2006
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Dissociation between alveolar transmigration of neutrophils and lung injury in hyperoxia

Sandra Perkowski,1,* Arnaud Scherpereel,2,4,* Juan-Carlos Murciano,3,5 Evguenia Arguiri,2 Charalambos C. Solomides,6 Steven M. Albelda,2 Vladimir Muzykantov,3 and Melpo Christofidou-Solomidou2

1School of Veterinary Medicine, 2Departments of Medicine and 3Pharmacology, University of Pennsylvania, Philadelphia, Pennsylvania; 4INSERM U774, Institut Pasteur de Lille, Lille, France; 5Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain; and 6Temple University Hospital, Department of Pathology, Philadelphia, Pennsylvania

Submitted 22 February 2006 ; accepted in final form 23 June 2006

The objective of this study was to quantitatively assess changes in cell adhesion molecule (CAM) expression on the pulmonary endothelial surface during hyperoxia and to assess the functional significance of those changes on cellular trafficking and development of oxygen-induced lung injury. Mice were placed in >95% O2 for 0–72 h, and pulmonary injury and neutrophil (PMN) sequestration were assessed. Specific pulmonary CAM expression was quantified with a dual-radiolabeled MAb technique. To test the role of CAMs in PMN trafficking during hyperoxia, blocking MAbs to murine P-selectin, ICAM-1, or platelet-endothelial cell adhesion molecule-1 (PECAM-1) were injected in wild-type mice. Mice genetically deficient in these CAMs and PMN-depleted mice were also evaluated. PMN sequestration occurred within 8 h of hyperoxia, although alveolar emigration occurred later (between 48 and 72 h), coincident with rapid escalation of the lung injury. Hyperoxia significantly increased pulmonary uptake of radiolabeled antibodies to P-selectin, ICAM-1, and PECAM-1, reflecting an increase in their level on pulmonary endothelium and possibly sequestered blood cells. Although both anti-PECAM-1 and anti-ICAM-1 antibodies suppressed PMN alveolar influx in wild-type mice, only mice genetically deficient in PECAM-1 showed PMN influx suppression. Neither CAM blockade, nor genetic deficiency, nor PMN depletion attenuated lung injury. We conclude that early pulmonary PMN retention during hyperoxia is not temporally associated with an increase in endothelial CAMs; however, subsequent PMN emigration into the alveolar space may be supported by PECAM-1 and ICAM-1. Blocking PMN recruitment did not prevent lung injury, supporting dissociation between PMN infiltration and lung injury during hyperoxia in mice.

cell adhesion molecules; ICAM-1; platelet-endothelial cell adhesion molecule-1; P-selectin; hyperoxia; pulmonary neutrophil depletion; acute lung injury


Address for reprint requests and other correspondence: M. Christofidou-Solomidou, Dept. of Medicine, Pulmonary, Allergy, and Critical Care Division, Univ. of Pennsylvania, 421 Curie Blvd., BRB II/III, Philadelphia, PA 19104 (e-mail: melpo{at}mail.med.upenn.edu)




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