期刊
JOURNAL OF INNATE IMMUNITY
卷 11, 期 6, 页码 457-468出版社
KARGER
DOI: 10.1159/000496403
关键词
Group A Streptococcus; Streptolysin O; Ubiquitin; IL-1 beta
类别
资金
- Swedish Foundation for Strategic Research
- Emil and Wera Cornell Foundation
- Crafoord Foundation
- Royal Physiographic Society of Lund
- Gyllenstierna Krapperup's Foundation
- HRH Crown Princess Lovisa's Pediatrics Association
- foundation of Magnus Bergvall
- foundation of Golje-Lundstrom
- foundation of Thelma Zoega
- foundation of Alfred Osterlund
- U.S. Public Health Service [AI070926, AI029952, AI07538, AI129527]
- Norwegian Cancer Society [B05035/001]
- Research Council of Norway Center of Excellence Funding Scheme project [223255/F50]
- foundation of Anna and Edwin Berger
Group A Streptococcus (GAS) is a common and versatile human pathogen causing a variety of diseases. One of the many virulence factors of GAS is the secreted pore-forming cytotoxin streptolysin O (SLO), which has been ascribed multiple properties, including inflammasome activation leading to release of the potent inflammatory cytokine IL-1 beta from infected macrophages. IL-1 beta is synthesized as an inactive pro-form, which is activated intracellularly through proteolytic cleavage. Here, we use a macrophage infection model to show that SLO specifically induces ubiquitination and degradation of pro-IL-1 beta. Ubiquitination was dependent on SLO being released from the infecting bacterium, and pore formation by SLO was required but not sufficient for the induction of ubiquitination. Our data provide evidence for a novel SLO-mediated mechanism of immune regulation, emphasizing the importance of this pore-forming toxin in bacterial virulence and pathogenesis.
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