TY - JOUR
T1 - RNA and beta;-hemolysin of group B streptococcus induce interleukin-1β (IL-1β) by activating NLRP3 inflammasomes in mouse macrophages
AU - Gupta, Rahul
AU - Ghosh, Shubhendu
AU - Monks, Brian
AU - DeOliveira, Rosane B.
AU - Tzeng, Te Chen
AU - Kalantari, Parisa
AU - Nandy, Anubhab
AU - Bhattacharjee, Bornali
AU - Chan, Jennie
AU - Ferreira, Fabianno
AU - Rathinam, Vijay
AU - Sharma, Shruti
AU - Lien, Egil
AU - Silverman, Neal
AU - Fitzgerald, Katherine
AU - Firon, Arnaud
AU - Trieu-Cuot, Patrick
AU - Henneke, Philipp
AU - Golenbock, Douglas T.
PY - 2014/5/16
Y1 - 2014/5/16
N2 - The inflammatory cytokine IL-1β is critical for host responses against many human pathogens. Here, we define Group B Strep-tococcus (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.
AB - The inflammatory cytokine IL-1β is critical for host responses against many human pathogens. Here, we define Group B Strep-tococcus (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.
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U2 - 10.1074/jbc.C114.548982
DO - 10.1074/jbc.C114.548982
M3 - Article
C2 - 24692555
AN - SCOPUS:84901020681
SN - 0021-9258
VL - 289
SP - 13701
EP - 13705
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
IS - 20
ER -