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Interactions of Rickettsia rickettsii with Endothelial Nuclear Factor‐κB in a “Cell‐Free” System

Vascular endothelial cells (EC) are the primary targets of in vivo infection with Rickettsia rickettsii , an obligate intracellular, gram-negative bacterial organism, and the etiological agent for Rocky Mountain spotted fever. Although infection of cultured human endothelial cells with R. rickettsii culminates in extensive membrane damage and necrotic death, 1 it has been established that the endothelial cell is not simply injured by infection, but undergoes a series of responses including functional changes characteristic of an “activated” phenotype. 2 In brief, the endothelial cells display procoagulant and proinflammatory properties during the course of infection, which likely contribute to the manifestation of disease symptoms. Nuclear factor-kappaB (NFκ B) is a dimeric transcription factor composed of homoand heterodimers of the Rel family of proteins (Rel A or p65, Rel B, c-Rel, NFκ B1 or p50, and NFκ B2 or p52). It is now known that NFκ B is present in the cytoplasm of virtually all eukaryotic cells as an inactive complex, bound to one of the members of I κ B (inhibitors of NFκ B) proteins. Stimulus-induced signaling cascades lead to the proteolysis of I κ B and release of active NFκ B, which translocates to the nucleus, binds to κ B enhancer sequences via the DNA-binding domain, and regulates the transcription of specific genes. 3 Our laboratory has shown that NFκ B governs important regulatory functions during R. rickettsii infection of cultured human EC, resulting in reprogramming of gene expression and suppression of apoptotic host cell death. 4,5