期刊
CELL REPORTS
卷 9, 期 3, 页码 910-917出版社
CELL PRESS
DOI: 10.1016/j.celrep.2014.10.003
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类别
资金
- Olympia-Morata Habilitation fellowship (University of Heidelberg)
- Medizinische Fakultat Heidelberg
- [SPP1468 IMMUNOBONE]
Bacterial components are recognized by the immune system through activation of the inflammasome, eventually causing processing of the proinflammatory cytokine interleukin-1 beta (IL-1 beta), a pleiotropic cytokine and one of the most important mediators of inflammation, through the protease caspase-1. Synthesis of the precursor protein and processing into its bioactive form are tightly regulated, given that disturbed control of IL-1 beta release can cause severe autoinflammatory diseases or contribute to cancer development. We show that the bacterial Pasteurella multocida toxin (PMT) triggers Il1b gene transcription in macrophages independently of Toll-like receptor signaling through RhoA/Rho-kinase-mediated NF-kappa B activation. Furthermore, PMT mediates signal transducer and activator of transcription (STAT) protein-controlled granzyme A (a serine protease) expression in macrophages. The exocytosed granzyme A enters target cells and mediates IL-1 beta maturation independently of caspase-1 and without inducing cytotoxicity. These findings show that macrophages can induce an IL-1 beta-initiated immune response independently of inflammasome activity.
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