RNA and {beta}-hemolysin of Group B streptococcus induce IL-1{beta} by activating NLRP3 inflammasomes in mouse macrophages [Signal Transduction]

April 1st, 2014 by Gupta, R., Ghosh, S., Monks, B., DeOliveira, R., Tzeng, T., Kalantari, P., Nandy, A., Bhattacharjee, B., Chan, J., Ferreira, F., Rathinam, V., Sharma, S., Lien, E., Silverman, N., Fitzgerald, K., Firon, A., Trieu-Cuot, P., Henneke, P., Golenbock, D.

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.
  • Posted in Journal of Biological Chemistry, Publications
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