Acute lung injury is the end result of common pathways initiated by a variety of local or systemic insults leading to diffuse damage to the pulmonary parenchyma. Despite the accumulation of abundant information regarding the physiological and cellular basis of lung injury and increasingly sophisticated intensive care, an improvement in prognosis has lagged behind. It has become clear that there is not one mediator responsible for acute lung injury but rather a complex interplay exists between diverse proinflammatory (eg, lipopolysaccharide, complement products, cytokines, chemokines, reactive oxygen species, and eicosanoids) and anti-inflammatory (interleukin- 10, interleukin-1 -RA, PGI2) mediators. It is essential that we obtain a better understanding of the complexities of the acute inflammatory response if we are to successfully intervene to prevent or ameliorate tissue injury. The purpose of this review is to summarize recent developments that have contributed to our understanding of the basic mechanisms of lung injury. We focus on the persistence of the inflammatory response on a local and systemic level, including local mechanisms acting within the alveolar space regulating synthesis, release, and activation of inflammatory mediators; the balance of proteinases and antiproteinases; the abnormalities of surfactant; and the potential importance of endogenously released anti-inflammatory mediators. It is hoped that the results of these studies will provide insights into the pathogenesis of lung injury and lead to novel therapeutic strategies to prevent or ameliorate lung injury.
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