Lipopolysaccharide from the periodontal pathogen Porphyromonas gingivalis prevents apoptosis of HL60-derived neutrophils in vitro.
Lipopolysaccharide (LPS) from Porphyromonas gingivalis prevented apoptosis of HL60-derived neutrophils, which could not be restored upon the addition of interleukin-10. Signaling of P. gingivalis LPS through Toll-like receptor 2 (TLR2), not TLR4, may account for the inhibiting effect of P. gingivalis LPS on apoptosis and provide a mechanism for the development of destructive periodontal inflammation.
Murray
D A
DA
Department of Adult Dental Health, Dental School, University of Wales College of Medicine, Heath Park, Cardiff CF4 4XY, United Kingdom.
Wilton
J M A
JM
D017209:Apoptosis / Q000187:drug effects*; D002460:Cell Line; D006801:Humans; D008070:Lipopolysaccharides / Q000494:pharmacology*; D009504:Neutrophils / Q000276:immunology*; D010510:Periodontal Diseases / Q000276:immunology / Q000382:microbiology; D016966:Porphyromonas gingivalis / Q000378:metabolism / Q000472:pathogenicity*
D008070:Lipopolysaccharides