ful to Dr. Elizabeth Lyimo who was responsible for collecting data in Tanzania. Pattern Recognition Receptor–Dependent Mechanisms of Acute Lung Injury Acute lung injury (ALI) that clinically manifests as acute respiratory distress syndrome is caused by an uncontrolled systemic inflammatory response resulting from clinical events including sepsis, major surgery and trauma. Innate immunity activation plays a central role in the development of ALI. Innate immunity is activated through families of related pattern recognition receptors (PRRs), which recognize conserved microbial motifs or pathogen-associated molecular patterns (PAMPs). Toll-like receptors were the first major family of PRRs discovered in mammals. Recently, NACHT–leucine-rich repeat (LRR) receptors and retinoic acid–inducible gene–like receptors have been added to the list. It is now understood that in addition to recognizing infectious stimuli, both Toll-like receptors and NACHT-LRR receptors can also respond to endogenous molecules released in response to stress, trauma and cell damage. These molecules have been termed damage-associated molecular patterns (DAMPs). It has been clinically observed for a long time that infectious and noninfectious insults initiate inflammation, so confirmation of overlapping receptor-signal pathways of activation between PAMPs and DAMPs is no surprise. This review provides an overview of the PRR-dependent mechanisms of ALI and clinical implication. Modification of PRR pathways is likely to be a logical therapeutic target for ALI/acute respiratory distress syndrome. (TLRs 1-9 and TLRs 11-13) in mice have been defined (14) . TLRs 3, 7, 8 and 9 are expressed intracellularly, whereas TLRs 1, 2, 4, 5, 6 and 10 are expressed on the cell surface. TLRs are expressed on a range of immune cells including macrophages, dendritic cells, B cells and certain types of T cells, as well as on certain nonimmune cells, such as endothelial cells, smooth muscle cells and epithelial cells that lie at potential sites of entry, including the skin and the respiratory, intestinal and genitourinary tracts. The expression of TLRs is modulated by activation, matu-ration or differentiation of the different cell types (15, 16) .