Abstract
Lipopolysaccharide (LPS) fromPorphyromonas gingivalisprevented apoptosis of HL60-derived neutrophils, which could not be restored upon the addition of interleukin-10. Signaling ofP. gingivalisLPS through Toll-like receptor 2 (TLR2), not TLR4, may account for the inhibiting effect ofP. gingivalisLPS on apoptosis and provide a mechanism for the development of destructive periodontal inflammation.

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