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Modulation of gene expression via disruption of NF-kappa B signaling by a bacterial small molecule

Academic Article
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Overview

authors

  • Kravchenko, Vladimir
  • Kaufmann, Gunnar
  • Mathison, J. C.
  • Scott, D. A.
  • Katz, A. Z.
  • Grauer, D. C.
  • Lehmann, M.
  • Meijler, M. M.
  • Janda, Kim
  • Ulevitch, Richard

publication date

  • 2008

journal

  • Science  Journal

abstract

  • The control of innate immune responses through activation of the nuclear transcription factor NF-kappaB is essential for the elimination of invading microbial pathogens. We showed that the bacterial N-(3-oxo-dodecanoyl) homoserine lactone (C12) selectively impairs the regulation of NF-kappaB functions in activated mammalian cells. The consequence is specific repression of stimulus-mediated induction of NF-kappaB-responsive genes encoding inflammatory cytokines and other immune regulators. These findings uncover a strategy by which C12-producing opportunistic pathogens, such as Pseudomonas aeruginosa, attenuate the innate immune system to establish and maintain local persistent infection in humans, for example, in cystic fibrosis patients.

subject areas

  • 4-Butyrolactone
  • Adult
  • Animals
  • Cyclic AMP Response Element-Binding Protein
  • Cystic Fibrosis
  • Female
  • Gene Expression Regulation
  • Homoserine
  • Humans
  • I-kappa B Kinase
  • I-kappa B Proteins
  • Immunity, Innate
  • Interferon-gamma
  • Lipopolysaccharides
  • Macrophage Activation
  • Macrophages
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Middle Aged
  • NF-kappa B
  • Phosphorylation
  • Pseudomonas Infections
  • Pseudomonas aeruginosa
  • Signal Transduction
  • Toll-Like Receptors
  • Transcription Factor RelA
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Identity

International Standard Serial Number (ISSN)

  • 0036-8075

Digital Object Identifier (DOI)

  • 10.1126/science.1156499

PubMed ID

  • 18566250
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Additional Document Info

start page

  • 259

end page

  • 263

volume

  • 321

issue

  • 5886

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