Type III secretion translocation pores of Yersinia enterocolitica trigger maturation and release of pro-inflammatory IL-1β

Authors


E-mail guy.cornelis@unibas.ch; Tel. (+41) 61 267 21 10; Fax (+41) 61 267 21 18.

Summary

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.

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