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

Vladimir V. Kravchenko, Gunnar F. Kaufmann, John C. Mathison, David A. Scott, Alexander Z. Katz, David C. Grauer, Mandy Lehmann, Michael M. Meijler, Kim D. Janda, Richard J. Ulevitch

Research output: Contribution to journalArticlepeer-review

189 Scopus citations

Abstract

The control of innate immune responses through activation of the nuclear transcription factor NF-κB 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-κB functions in activated mammalian cells. The consequence is specific repression of stimulus-mediated induction of NF-κB-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.

Original languageEnglish
Pages (from-to)259-263
Number of pages5
JournalScience
Volume321
Issue number5886
DOIs
StatePublished - 11 Jul 2008

ASJC Scopus subject areas

  • General

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