Downregulation of the DNA-binding activity of nuclear factor-kappaB p65 subunit in Porphyromonas gingivalis fimbria-induced tolerance

Infect Immun. 2004 Feb;72(2):1188-91. doi: 10.1128/IAI.72.2.1188-1191.2004.

Abstract

Porphyromonas gingivalis fimbriae induce high levels of nuclear factor-kappaB (NF-kappaB)-dependent cytokine release upon primary but not secondary stimulation of monocytic cells (FimA tolerance). In this study, fimbriae induced Toll-like receptor-mediated activation of both p50 and p65 subunits of NF-kappaB upon primary cellular activation. However, activation of the transactivating p65 subunit (but not of the transcriptionally inactive p50 subunit) was significantly inhibited in fimbria-restimulated cells. Moreover, expression of a NF-kappaB-dependent reporter gene was inhibited upon secondary stimulation with fimbriae. NF-kappaB p65 downregulation may thus contribute to induction of FimA tolerance.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • CHO Cells
  • Cell Line
  • Cricetinae
  • DNA / metabolism*
  • Down-Regulation
  • Fimbriae Proteins / pharmacology
  • Fimbriae, Bacterial / physiology*
  • Humans
  • Membrane Glycoproteins / physiology
  • NF-kappa B / metabolism*
  • Porphyromonas gingivalis / physiology*
  • Receptors, Cell Surface / physiology
  • Receptors, Interleukin-2 / biosynthesis
  • Recombinant Proteins / pharmacology
  • Toll-Like Receptors
  • Transcription Factor RelA

Substances

  • Membrane Glycoproteins
  • NF-kappa B
  • Receptors, Cell Surface
  • Receptors, Interleukin-2
  • Recombinant Proteins
  • Toll-Like Receptors
  • Transcription Factor RelA
  • fimbrillin
  • Fimbriae Proteins
  • DNA