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The Role of Chemokines in the Pathophysiology of the Acute Respiratory Distress Syndrome (ARDS)

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Part of the book series: Contemporary Immunology ((CONTIM))

Abstract

The acute respiratory distress syndrome (ARDS) is an acute life-threatening illness characterized by the rapid onset of severe respiratory failure, usually following sepsis, trauma, or other clinical events. The clinical hallmarks of ARDS are diffuse bilateral pulmonary infiltrates, critical hypoxemia, and normal intracardiac filling pressures (1). The underlying pathophysiologic mechanism is severe and diffuse injury to the epithelial and endothelial barriers in the lungs, and flooding of the airspaces with a proteinaceous fibrin-rich exudate. Since the first description of ARDS, it has been suspected that acute inflammatory mechanisms in the lungs played an important role in the pathogenesis of the disease. Studies using bronchoalveolar lavage (BAL) to sample the airspaces of affected patients have consistently shown that the intrapulmonary inflammatory response is characterized by the accumulation of polymorphonuclear leukocytes (PMN), protein, and a variety of pro- and anti-inflammatory mediators in the airspaces of the lungs.

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Martin, T.R., Goodman, R.B. (1999). The Role of Chemokines in the Pathophysiology of the Acute Respiratory Distress Syndrome (ARDS). In: Hébert, C.A. (eds) Chemokines in Disease. Contemporary Immunology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-706-2_6

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