| Literature DB >> 20114027 |
Takahiro Shimada1, Bong Goo Park, Andrea J Wolf, Constantinos Brikos, Helen S Goodridge, Courtney A Becker, Christopher N Reyes, Edward A Miao, Alan Aderem, Friedrich Götz, George Y Liu, David M Underhill.
Abstract
IL-1beta produced by phagocytes is important for protection against the mucosal pathogen Staphylococcus aureus. Processing and maturation of this cytokine requires activation of the multiprotein inflammasome complex. We observed that the bacterial cell wall component peptidoglycan (PGN) must be particulate and internalized via phagocytosis to activate NLRP3 inflammasomes and IL-1beta secretion. In the context of S. aureus infection of macrophages, we find that phagocytosis and lysozyme-based bacterial cell wall degradation are necessary to induce IL-1beta secretion. Further, an S. aureus enzyme, PGN O-acetyltransferase A, previously demonstrated to make cell wall PGN resistant to lysozyme, strongly suppresses inflammasome activation and inflammation in vitro and in vivo. These observations demonstrate that phagocytosis and lysozyme-based cell wall degradation of S. aureus are functionally coupled to inflammasome activation and IL-1beta secretion and illustrate a case whereby a bacterium specifically subverts IL-1beta secretion through chemical modification of its cell wall PGN. 2010 Elsevier Inc. All rights reserved.Entities:
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Year: 2010 PMID： 20114027 PMCID： PMC2818986 DOI： 10.1016/j.chom.2009.12.008
Source DB: PubMed Journal: Cell Host Microbe ISSN： 1931-3128 Impact factor: 21.023