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. gingivali...

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Veröffentlicht in:Infection and immunity Jg. 71; H. 12; S. 7232
Hauptverfasser: Murray, D A, Wilton, J M A
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 01.12.2003
Schlagworte:
Apoptosis - drug effects
Cell Line
Humans
Lipopolysaccharides - pharmacology
Neutrophils - immunology
Periodontal Diseases - immunology
Periodontal Diseases - microbiology
Porphyromonas gingivalis - metabolism
Porphyromonas gingivalis - pathogenicity
ISSN:0019-9567
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Zusammenfassung: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.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:0019-9567
DOI:10.1128/IAI.71.12.7232-7235.2003