First Author | van der Velden AW | Year | 2003 |
Journal | J Immunol | Volume | 171 |
Issue | 12 | Pages | 6742-9 |
PubMed ID | 14662878 | Mgi Jnum | J:118499 |
Mgi Id | MGI:3699682 | Doi | 10.4049/jimmunol.171.12.6742 |
Citation | van der Velden AW, et al. (2003) Salmonella rapidly kill dendritic cells via a caspase-1-dependent mechanism. J Immunol 171(12):6742-9 |
abstractText | Dendritic cells provide a critical link between innate and acquired immunity. In this study, we demonstrate that the bacterial pathogen Salmonella enterica serovar Typhimurium can efficiently kill these professional phagocytes via a mechanism that is dependent on sipB and the Salmonella pathogenicity island 1-encoded type III protein secretion system. Rapid phosphatidylserine redistribution, caspase activation, and loss of plasma membrane integrity were characteristic of dendritic cells infected with wild-type Salmonella, but not sipB mutant bacteria. Caspase-1 was particularly important in this process because Salmonella-induced dendritic cell death was dramatically reduced in the presence of a caspase-1-specific inhibitor. Furthermore, dendritic cells obtained from caspase-1-deficient mice, but not heterozygous littermate control mice, were resistant to Salmonella-induced cytotoxicity. We hypothesize that Salmonella have evolved the ability to selectively kill professional APCs to combat, exploit, or evade immune defense mechanisms. |