Type III secretion translocation pores of Yersinia enterocolitica trigger maturation and release of pro-inflammatory IL-1β
Article first published online: 20 JUN 2007
Volume 9, Issue 12, pages 2893–2902, December 2007
How to Cite
Shin, H. and Cornelis, G. R. (2007), Type III secretion translocation pores of Yersinia enterocolitica trigger maturation and release of pro-inflammatory IL-1β. Cellular Microbiology, 9: 2893–2902. doi: 10.1111/j.1462-5822.2007.01004.x
- Issue published online: 13 AUG 2007
- Article first published online: 20 JUN 2007
- Received 13 April, 2007; revised 13 June, 2007; accepted 13 June, 2007.
Bacteria from the genus Yersinia deliver a number of effectors into host cells via type III secretion (T3S). Injected Yop effectors interfere and prevent pro-inflammatory warning signals by hijacking the host's intracellular machinery. While macrophages infected by wild-type Yersinia enterocolitica did not release mature IL-1β, macrophages infected by Y. enterocolitica deprived of all effectors released mature IL-1β. Surprisingly, macrophages infected by Y. enterocolitica deficient for secretion of all T3S proteins, including effectors and translocators, did not release mature IL-1β. Using different genetic constructs, we show that insertion of T3S translocation pores trigger activation of caspase-1, maturation of proIL-1β and release of mature IL-1β, which occurs independently of cell osmotic lysis. These data show that T3S translocation is intrinsically a pro-inflammatory phenomenon. However, in the case of Yersinia, this effect is neutralized by the action of effectors.