Th e truncated form of full-length RAGE, soluble RAGE (sRAGE), consists of only the extracellular ligand-binding domain (V-C-C') lacking the cytosolic and trans membrane domains (i.e., the parts that transfer a signal into the cell) and circulates in the bloodstream. sRAGE has been indicated to be involved in infl ammatory processes in several ways. First, sRAGE blood concentrations are associated with various infl ammatory diseases in patients and in rats with experimentally induced ALI [29] . Further more, it is suggested that sRAGE can compete with full length cell-surface RAGE for ligand engagement, preventing these ligands from binding to RAGE or other receptors and/or exerting eff ects otherwise. Exogenous sRAGE treatment indeed attenuated infl ammatory responses in several animal models, including models of type II collagen-induced arthritis, hepatic injury, diabetic atherosclerosis, delayed type hypersensitivity, and experimental auto-immune encephalomyelitis [7] . Th e involvement of sRAGE during infection is not known. Based on experimental studies in rats and in patients with ALI, sRAGE has been described as a marker of lung injury [29] .