作者: Matthew J. Sullivan , Sophie Y. Leclercq , Deepak S. Ipe , Alison J. Carey , Joshua P. Smith
关键词: Streptococcus agalactiae 、 Hemolysin 、 Pathogenesis 、 Cytolysin 、 Biology 、 Wild type 、 Bacterial adhesin 、 Microbiology 、 Inflammation 、 Virulence 、 Immunology
摘要: Background - Streptococcus agalactiae can cause urinary tract infection (UTI). The role of the S. global virulence regulator, CovR, in UTI pathogenesis is unknown Methods We used murine and human bladder uroepithelial cell models mutants covR related factors, including -hemolysin/cytolysin ( -h/c), surface-anchored adhesin HvgA, capsule to study CovR UTI. Results covR-deficient serotype III 874391 was significantly attenuated for colonization mice adhesion cells. Mice infected with produced less pro-inflammatory cytokines compared wild type (WT) 874391. Acute cytotoxicity cells triggered by but not WT associated significant caspase-3 activation. Mechanistically, mutation altered expression several genes that encode key -h/c capsule. Subsequent mutational analyses revealed HvgA capsule, -h/c, exerted effects on vivo. Conclusion promotes inflammation, viability complex, multifactorial influenced