ABSTRACT
I. Introduction Many clinical entities, including trauma, pneumonia/sepsis, ischemia-reperfusion injury, as well as ARDS, are characterized by varying degrees of acute pulmonary inflammation. This inflammatory response is initiated, maintained, resolves, and depends upon a complex yet coordinated intercellular interaction between immune and nonimmune cells. For example, the host response to bacterial pneumonia is characterized by acute inflammation and once the inciting microbe is cleared the inflammatory reaction resolves and normal repair and tissue remodeling occurs. This re-establishes normal lung function without the sequela of chronic inflammation and pulmonary fibrosis. In contrast, the acute inflammatory response associated with ARDS may culminate in severe lung injury, ultimately impairing lung function and impacting on host survival.
