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• W2019988013 abstract "Production of IL-1beta 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-1beta 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-1beta gene and intracellular accumulation of IL-1beta protein. However, IL-1beta 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-1beta secretion in infected cells. The Nalp3 inflammasome is therefore likely to be an important mediator of the inflammatory response in gingival epithelium." @default.
• W2019988013 created "2016-06-24" @default.
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• W2019988013 date "2010-02-01" @default.
• W2019988013 modified "2023-09-26" @default.
• W2019988013 title "ATP-dependent activation of an inflammasome in primary gingival epithelial cells infected by<i>Porphyromonas gingivalis</i>" @default.
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• W2019988013 doi "https://doi.org/10.1111/j.1462-5822.2009.01390.x" @default.
• W2019988013 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2807919" @default.
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