Dissociation between alveolar transmigration of neutrophils and lung injury in hyperoxia.

Dissociation between alveolar transmigration of neutrophils and lung injury in hyperoxia. Research Abstract Details 

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Dissociation between alveolar transmigration of neutrophils and lung injury in hyperoxia. Abstract Text:

Sandra Perkowski,Arnaud Scherpereel,Juan-Carlos Murciano,Evguenia Arguiri,Charalambos C Solomides,Steven M Albelda,Vladimir Muzykantov,Melpo Christofidou-Solomidou,

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% O(2) 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.

Dissociation between alveolar transmigration of neutrophils and lung injury in hyperoxia. Publishing Authors By Initials

S Perkowski,A Scherpereel,JC Murciano,E Arguiri,CC Solomides,SM Albelda,V Muzykantov,M Christofidou-Solomidou,

For similar respiratory tract diseases: lung diseases: respiratory distress syndrome, adult research abstracts see: respiratory tract diseases: lung diseases: respiratory distress syndrome, adult research

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Dissociation between alveolar transmigration of neutrophils and lung injury in hyperoxia. Journal Published:

PUBLICATION TYPE: Research Support, U.S. Gov't,

Journal: American journal of physiology. Lung cellular and

VOLUME: 291

Page Numbers: L1050-8

Journal Abbreviation: Am. J. Physiol. Lung Cell Mol.

ISSN: 1040-0605

DAY: 30

MONTH: 06

YEAR: 2006

Dissociation between alveolar transmigration of neutrophils and lung injury in hyperoxia. Information

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LANGUAGE: eng

NlmUniqueID: 100901229

Dissociation between alveolar transmigration of neutrophils and lung injury in hyperoxia. Keywords Mesh Terms:

KEYWORDS: Respiratory Distress Syndrome, Adult

MESH TERMS: pathology

Chemical & Substance for Abstract: Dissociation between alveolar transmigration of neutrophils and lung injury in hyperoxia. Information

Substance Name: Oxygen

Registry Number: 7782-44-7

Grant and Affiliation Information for Dissociation between alveolar transmigration of neutrophils and lung injury in hyperoxia.

AFFILIATION: School of Veterinary Medicine, University of Pennsylvania, 421 Curie Blvd., BRB II/III, Philadelphia, 19104, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: R01 HL-071174

ACRONYM: HL

MEDLINETA: Am J Physiol Lung Cell Mol Phy

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