Type III secretion translocation pores of Yersinia enterocolitica trigger maturation and release of pro-inflammatory IL-1beta.
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-1beta, macrophages infected by Y. enterocolitica deprived of all effectors released mature IL-1beta. Surprisingly, macrophages infected by Y. enterocolitica deficient for secretion of all T3S proteins, including effectors and translocators, did not release mature IL-1beta. Using different genetic constructs, we show that insertion of T3S translocation pores trigger activation of caspase-1, maturation of proIL-1beta and release of mature IL-1beta, 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.
Shin
Hwain
H
Biozentrum, University of Basel, Basel, Switzerland.
Cornelis
Guy R
GR
D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics / Q000276:immunology*; D002352:Carrier Proteins / Q000235:genetics / Q000276:immunology*; D020170:Caspase 1 / Q000096:biosynthesis; D002460:Cell Line; D006801:Humans; D053583:Interleukin-1beta / Q000276:immunology* / Q000378:metabolism*; D008264:Macrophages / Q000276:immunology; D051379:Mice; D015008:Yersinia enterocolitica / Q000276:immunology*
D001426:Bacterial Proteins; D002352:Carrier Proteins; D053583:Interleukin-1beta; D020170:Caspase 1