Signaling interactions between vascular endothelium and invading rickettsiae provide a unique way of coordinating appropriate physiologic responses, which are important determinants of the ensuing pathogenesis mechanisms such as host defense and inflammation. Two major subgroups of pathogenic Rickettsia species, namely the typhus group (TG) and the spotted fever group (SFG), exhibit marked differences in their intracytoplasmic behavior. Using in vitro infection of cultured human endothelial cells with R. rickettsii, the causative agent of Rocky Mountain SF, we previously identified activation of NF-kappaB and p38 MAP kinase as essential components of intracellular signaling events responsible for Rickettsia-induced transcriptional activation. Our data also suggest that p38 activity does not contribute to NF-kappaB response, implicating involvement of independent upstream signaling pathways. Since divergent cytopathologies suggest potentially different interactions with host cells, the aim of this study was to compare these responses after endothelial cell infection with R. conorii, the agent of Mediterranean SF, and a TG representative R. typhi, the agent of endemic typhus.
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)