In:
The Journal of Immunology, The American Association of Immunologists, Vol. 182, No. 1_Supplement ( 2009-04-01), p. 134.38-134.38
Abstract:
IL-1β produced by phagocytes is important for protection against Staphylococcus aureus, a bacterium that causes serious skin and invasive diseases and is contributing to a current public health crisis due to the emergence of methicillin-resistant strains. Secretion of IL-1β requires both activation of a transcriptional signal to stimulate production of pro- IL-1β, (usually provided by TLR signaling) and a second signal to stimulate processing by inflammasome complexes and release of the mature cytokine. We show here that phagocytosis and lysozyme-based degradation of bacterial cell walls are functionally coupled to activation of Nalp3 inflammasomes and secretion of IL-1β in response to live S. aureus and to S. aureus peptidoglycan. Further, a S. aureus peptidoglycan-modifying enzyme that makes its peptidoglycan resistant to lysozyme strongly suppresses inflammasome activation. This is the first demonstration of a case whereby a bacterium avoids IL-1β secretion through chemical modification of its cell wall peptidoglycan, and we hypothesize that this reduced IL-1β production is key to successful mucosal colonization and infection. This research is supported by grants from NIGMS and the American Heart Association.
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.182.Supp.134.38
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2009
detail.hit.zdb_id:
1475085-5
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