Molecular determinants of LPS-induced acute renal inflammation: Implication of the kinin B1 receptor

Acute renal inflammation represents a complex disease and its molecular basis remains incompletely defined. We examined changes of global renal gene expression in lipopolysacharide-treated wild-type and kinin B1 receptor-knockout mice to better comprehend molecular mechanisms of acute renal inflammation and possible implications of the kinin B1 receptor in early (inflammatory) stages of renal disease. Microarray data revealed that LPS-mediated renal inflammation is associated with strong induction of gene families that are mostly involved in inflammatory and immune response and cell adhesion, as well as genes associated with metabolism, signal transduction and transport. Downregulated by the LPS challenge were genes and pathways that are necessary for normal renal function, including those implicated in metabolism, transport, protein biosynthesis and, cytoskeleton organization, regulation of transcription and signal transduction. Moreover, we show that B1 receptor ablation could be protective against inflammation-related kidney injuries.