Minimal SPI1-T3SS effector requirement for Salmonella enterocyte invasion and intracellular proliferation in vivo

摘要: Effector molecules translocated by the Salmonella pathogenicity island (SPI)1-encoded type 3 secretion system (T3SS) critically contribute to pathogenesis of human infection. They facilitate internalization non-phagocytic enterocytes rendering intestinal epithelium an entry site for Their function in vivo has remained ill-defined due lack a suitable animal model that allows visualization intraepithelial Salmonella. Here, we took advantage our novel neonatal mouse and analyzed various bacterial mutants reporter strains as well gene deficient mice. Our results demonstrate critical but redundant role SopE2 SipA enterocyte invasion, prerequisite transcriptional stimulation mucosal translocation vivo. In contrast, generation replicative endosomal compartment required cooperative action or SopB was independent SopA host MyD88 signaling. Intraepithelial growth had no influence on systemic spread. define SPI1-T3SS effector during invasion proliferation providing insight early course