The Role Of A-to-I ADAR1 Of Alveolar Macrophage In LPS-induced Rat Acute Lung Injury

Multiple events, especially serious infections, are implicated as risk factors in the development of acute lung injury (ALI). It can develop to acute respiratory distress syndrome (ARDS) and companied with multiple organ failure (MOF) in late phase due to non-timely or inappropriate therapy. Bad outcome and high mortality rate (50-60%) are always the case attributed to lack of effective therapy. Lipopolysaccharide (LPS) is one of the most important causative agents which induced ALI and the mechanism is still unclear. Attention has focused on the potential role of polymorphonuclear neutrophils (PMNs) during the development of ALI in the past years, while ALI still happened in neutropenic patients. The study of macrophages in the development of ALI has been carried out in recent years. Increased alveolar macrophages (AMs) have been detected in ALI in early stage and released numerous inflammatory mediators, such as TNF, IL-1, 6, 8 and PAF, which appear to participate in lung inflammation and injury by acting on PMNs and endothelia cells. While, the cellular sources of these mediators and the manner by which these mediators induce lung injury have yet to be elucidated. This initial introduction of the release of inflammatory mediators when macrophages induced by LPS "primed" the lung injury.