Open AccessType III secretion translocation pores of Yersinia enterocolitica trigger maturation and release of pro‐inflammatory IL‐1β
Author(s) -
Shin Hwain,
Cornelis Guy R.
Publication year - 2007
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2007.01004.x
Subject(s) - yersinia enterocolitica , secretion , effector , yersinia , biology , chromosomal translocation , microbiology and biotechnology , intracellular , bacteria , biochemistry , genetics , gene
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.