Journal
INNATE IMMUNITY
Volume 21, Issue 1, Pages 65-72Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/1753425914523459
Keywords
Inflammasome; Porphyromonas gingivalis; endothelial; inflammation; atherosclerosis; NLRP3
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Porphyromonas gingivalis (Pg) is involved in the link between periodontal diseases and atherosclerosis worsening. In periodontal cells, Pg modifies IL-1 expression via the NLRP3 inflammasome pathway activation. Our aim was to investigate NLRP3 inflammasome activation in endothelial cells (ECs) after Pg infection and Pg-LPS stimulation. In both situations, RT-PCR experiments demonstrated an increase of the NLRP3 mRNA level that can be potentiated by pre-treatment of ECs with 5mM ATP. However, Western blotting analysis revealed that Pg infection induced a proteolysis of NLRP3 protein and a major decrease of the native protein. After ATP pre-treatment and/or Pg-LPS stimulation, this proteolysis was not observed, while NLRP3 protein levels were increased. Proteolysis of the NLRP3 protein was not observed with heat-killed Pg and inhibition of ECs protein synthesis with cycloheximide did not abolish the NLRP3 protein degradation induced by Pg infection in ATP pre-treated cells. Additionally, significant increases of secreted IL-1 were measured after ATP pre-treatment and/or Pg-LPS stimulation, but not after Pg infection. These data showed that Pg and Pg-LPS differentially controlled the NLRP3 inflammasome pathway in ECs, and suggested a novel potential mechanism developed by Pg to reduce IL-1 secretion and to escape host immune response.
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