期刊
CELLULAR MICROBIOLOGY
卷 12, 期 2, 页码 188-198出版社
WILEY
DOI: 10.1111/j.1462-5822.2009.01390.x
关键词
-
资金
- NIDCR [R01DE016593, R01DE019444]
Production of IL-1 beta typically requires two-separate signals. The first signal, from a pathogen-associated molecular pattern, promotes intracellular production of immature cytokine. The second signal, derived from a danger signal such as extracellular ATP, results in assembly of an inflammasome, activation of caspase-1 and secretion of mature cytokine. The inflammasome component, Nalp3, plays a non-redundant role in caspase-1 activation in response to ATP binding to P2X(7) in macrophages. Gingival epithelial cells (GECs) are an important component of the innate-immune response to periodontal bacteria. We had shown that GECs express a functional P2X(7) receptor, but the ability of GECs to secrete IL-1 beta during infection remained unknown. We find that GECs express a functional Nalp3 inflammasome. Treatment of GECs with LPS or infection with the periodontal pathogen, Porphyromonas gingivalis, induced expression of the il-1 beta gene and intracellular accumulation of IL-1 beta protein. However, IL-1 beta was not secreted unless LPS-treated or infected cells were subsequently stimulated with ATP. Conversely, caspase-1 is activated in GECs following ATP treatment but not P. gingivalis infection. Furthermore, depletion of Nalp3 by siRNA abrogated the ability of ATP to induce IL-1 beta secretion in infected cells. The Nalp3 inflammasome is therefore likely to be an important mediator of the inflammatory response in gingival epithelium.
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