The acute respiratory distress syndrome (ARDS) is a process of acute inflammatory lung injury that affects a diverse array of surgical and medical patients. The syndrome is mediated by a complex and interacting system of chemical mediators produced by several types of pulmonary cells. Regardless of the predisposing causes, activation of the nuclear factor kappa B seems to be, at the molecular level, a signature event of ARDS, leading to the rapid activation of intracellular signaling pathways, which coordinate the induction of multiple genes encoding inflammatory mediators. There are at least two compelling reasons for promoting an understanding of these interactions and their molecular mediators and second messengers: new therapies intended to modulate these factors continue to be developed, and the levels of some of these molecules, most notably cytokines, may serve as early indicators of the onset of ARDS.