Our results demonstrate that Epac1-mediated signaling represents a mechanism for host-pathogen interactions and that Epac1 is a potential target for the prevention and treatment of fatal rickettsioses.
While bioinformatics analysis of the <i>C. felis</i> transcriptome identified homologs to all of the <i>Drosophila</i> immune deficiency (IMD) and Toll pathway components, an AMP gene expression profile in <i>Drosophila</i> cells indicated IMD pathway activation upon rickettsial infection.Accordingly, we assessed <i>R. typhi</i>-mediated flea IMD pathway activation <i>in vivo</i> using small interfering RNA (siRNA)-mediated knockdown.
While bioinformatics analysis of the <i>C. felis</i> transcriptome identified homologs to all of the <i>Drosophila</i> immune deficiency (IMD) and Toll pathway components, an AMP gene expression profile in <i>Drosophila</i> cells indicated IMD pathway activation upon rickettsial infection.Accordingly, we assessed <i>R. typhi</i>-mediated flea IMD pathway activation <i>in vivo</i> using small interfering RNA (siRNA)-mediated knockdown.
Together, these results identify host cell FGFR1 and rickettsial OmpA as another novel receptor-ligand pair contributing to the internalization of pathogenic rickettsiae into host endothelial cells and the potential application of FGFR-inhibitor drugs as adjunct therapeutics against spotted fever rickettsioses.
In this case, both the C-reactive protein and white blood cell count levels were lower than the ranges of these parameters for patients diagnosed with rickettsiosis.
Furthermore, our identification of lineage-specific Arf-GEF utilization across some rickettsial species illustrates different pathogenicity factors that define diverse agents of rickettsial diseases.
Furthermore, our identification of lineage-specific Arf-GEF utilization across some rickettsial species illustrates different pathogenicity factors that define diverse agents of rickettsial diseases.
All these observations raise an intriguing hypothesis about a novel cytoplasmic role of ANG, which is induced upon infection with Rickettsia and generates tRFs that may play roles in SFG rickettsioses.
Based on the emerging importance of the wingless (Wnt) pathways in inflammation and vascular biology, we hypothesized that Dickkopf-1 (DKK-1), as a major modulator of Wnt signaling, could be involved in the pathogenesis in rickettsial infections.
Intralesional expression of mRNA of interferon- gamma , tumor necrosis factor- alpha , interleukin-10, nitric oxide synthase, indoleamine-2,3-dioxygenase, and RANTES is a major immune effector in Mediterranean spotted fever rickettsiosis.
Induction of the endothelial COX-2 system and the resultant enhanced release of vasoactive PGs may contribute to the regulation of inflammatory responses and vascular permeability changes during spotted fever rickettsioses.
We evaluated whether TLR4 genotype is a component of genetic background protective versus rickettsiosis and whether this background influences longevity.
Induction of the endothelial COX-2 system and the resultant enhanced release of vasoactive PGs may contribute to the regulation of inflammatory responses and vascular permeability changes during spotted fever rickettsioses.
Induction of the endothelial COX-2 system and the resultant enhanced release of vasoactive PGs may contribute to the regulation of inflammatory responses and vascular permeability changes during spotted fever rickettsioses.