Yersinia enterocolitica Inhibits Salmonella enterica Serovar Typhimurium and Listeria monocytogenes Cellular Uptake

Abstract

ABSTRACTYersinia enterocoliticabiovar 1B employs two type three secretion systems (T3SS), Ysa and Ysc, which inject effector proteins into macrophages to prevent phagocytosis. Conversely,Salmonella entericaserovar Typhimurium uses a T3SS encoded bySalmonellapathogenicity island 1 (SPI1) to actively invade cells that are normally nonphagocytic and a second T3SS encoded by SPI2 to survive within macrophages. Given the distinctly different outcomes that occur with regard to host cell uptake ofS. Typhimurium andY. enterocolitica, we investigated how each pathogen influences the internalization outcome of the other.Y. enterocoliticareducesS. Typhimurium invasion of HeLa and Caco-2 cells to a level similar to that observed using anS. Typhimurium SPI1 mutant alone. However,Y. enterocoliticahad no effect onS. Typhimurium uptake by J774.1 or RAW264.7 macrophage-like cells.Y. enterocoliticawas also able to inhibit the invasion of epithelial and macrophage-like cells byListeria monocytogenes.Y. enterocoliticamutants lacking either the Ysa or Ysc T3SS were partially defective, while double mutants were completely defective, in blockingS. Typhimurium uptake by epithelial cells.S. Typhimurium encodes a LuxR homolog, SdiA, which detectsN-acylhomoserine lactones (AHLs) produced byY. enterocoliticaand upregulates the expression of an invasin (Rck) and a putative T3SS effector (SrgE). Two different methods of constitutively activating theS. Typhimurium SdiA regulon failed to reverse the uptake blockade imposed byY. enterocolitica.