Format

Send to

Choose Destination
J Biol Chem. 2014 May 16;289(20):13701-5. doi: 10.1074/jbc.C114.548982. Epub 2014 Apr 1.

RNA and β-hemolysin of group B Streptococcus induce interleukin-1β (IL-1β) by activating NLRP3 inflammasomes in mouse macrophages.

Author information

1
From the Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts 01605.
2
the Laboratório de Inflamação e Imunidade, Departamento de Imunologia, Instituto de Microbiologia, Universidade Federal do Rio de Janeiro (UFRJ), 21941-902 Rio de Janeiro, Brazil, and.
3
the Institut Pasteur, Unité de Biologie des Bactéries Pathogènes à Gram-Positif, 75724 Paris Cedex 15, France.
4
the Center of Chronic Immunodeficiency and Center of Pediatrics and Adolescent Medicine, University Medical Center Freiburg, 79106 Freiburg im Breisgau, Germany.
5
From the Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, Douglas.Golenbock@umassmed.edu.

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.

KEYWORDS:

Cell Signaling; Immunology; Innate Immunity; Interleukin; RNA

PMID:
24692555
PMCID:
PMC4022842
DOI:
10.1074/jbc.C114.548982
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for HighWire Icon for PubMed Central
Loading ...
Support Center