| Literature DB >> 24692555 |
Rahul Gupta1, Shubhendu Ghosh1, Brian Monks1, Rosane B DeOliveira1, Te-Chen Tzeng1, Parisa Kalantari1, Anubhab Nandy1, Bornali Bhattacharjee1, Jennie Chan1, Fabianno Ferreira2, Vijay Rathinam1, Shruti Sharma1, Egil Lien1, Neal Silverman1, Katherine Fitzgerald1, Arnaud Firon3, Patrick Trieu-Cuot3, Philipp Henneke4, Douglas T Golenbock5.
Abstract
The inflammatory cytokine IL-1β is critical for host responses against many human pathogens. Here, we define Group B Streptococcus (GBS)-mediated activation of the Nod-like receptor-P3 (NLRP3) inflammasome in macrophages. NLRP3 activation requires GBS expression of the cytolytic toxin, β-hemolysin, lysosomal acidification, and leakage. These processes allow the interaction of GBS RNA with cytosolic NLRP3. The present study supports a model in which GBS RNA, along with lysosomal components including cathepsins, leaks out of lysosomes and interacts with NLRP3 to induce IL-1β production.Entities:
Keywords: Cell Signaling; Immunology; Innate Immunity; Interleukin; RNA
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Year: 2014 PMID: 24692555 PMCID: PMC4022842 DOI: 10.1074/jbc.C114.548982
Source DB: PubMed Journal: J Biol Chem ISSN: 0021-9258 Impact factor: 5.157