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Role of platelet-activating factor in acid-induced lung injury
Abstracts / Prostaglandins & other Lipid Mediators 59 (1999) l-235
ROLE OF PLATELET-ACTIVATING
203
FACTOR IN ACID-INDUCED LUNG INJURY
Satoshi Ishii’, Takahide Nagase* and Takao Shimizu’ ‘Department of Biochemistry and Molecular Biology ‘Department of Geriatrics, Faculty of Medicine, The University of Tokyo, 7-3- 1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan Adult respiratory distress syndrome (ARDS) is an acute lung injury of high mortality rate and its mechanism is little known. Acid aspiration-induced lung injury is one of the most important causes of ARDS, characterized by an increase in lung permeability, enhanced polymorphonuclear neutrophil (PMN) sequestration and respiratory failure. Here, we investigated the role of platelet-activating factor (PAF) in the acid aspiration-induced lung injury by using two mutant mice, i.e., PAF receptor-overexpressing mice (Ishii, et al., (1997) EMBO J. 16: 133-142) and PAF receptor-deficient mice (Ishii et al. (1998) J. Exp. Med. 187: 1779-1788). When Hcl was given intratracheally, PAF receptor-overexpressing mice showed more severe lung injury, pulmonary edema and deterioration of gas exchange compare to wild-type mice. The current observations suggest PAF is involved in the pathogenesis of acute lung injury caused by acid aspiration, and that PMN infiltration is not sufficient to cause the lung injury.
ROLE OF PLATELET-ACTIVATING
203
FACTOR IN ACID-INDUCED LUNG INJURY
Satoshi Ishii’, Takahide Nagase* and Takao Shimizu’ ‘Department of Biochemistry and Molecular Biology ‘Department of Geriatrics, Faculty of Medicine, The University of Tokyo, 7-3- 1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan Adult respiratory distress syndrome (ARDS) is an acute lung injury of high mortality rate and its mechanism is little known. Acid aspiration-induced lung injury is one of the most important causes of ARDS, characterized by an increase in lung permeability, enhanced polymorphonuclear neutrophil (PMN) sequestration and respiratory failure. Here, we investigated the role of platelet-activating factor (PAF) in the acid aspiration-induced lung injury by using two mutant mice, i.e., PAF receptor-overexpressing mice (Ishii, et al., (1997) EMBO J. 16: 133-142) and PAF receptor-deficient mice (Ishii et al. (1998) J. Exp. Med. 187: 1779-1788). When Hcl was given intratracheally, PAF receptor-overexpressing mice showed more severe lung injury, pulmonary edema and deterioration of gas exchange compare to wild-type mice. The current observations suggest PAF is involved in the pathogenesis of acute lung injury caused by acid aspiration, and that PMN infiltration is not sufficient to cause the lung injury.