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2008:
Kravchenko Vladimir V; Kaufmann Gunnar F; Mathison John C; Scott David A; Katz Alexander Z; Grauer David C; Lehmann Mandy; Meijler Michael M; Janda Kim D; Ulevitch Richard J
Modulation of gene expression via disruption of NF-kappaB signaling by a bacterial small molecule.
Science (New York, N.Y.) 2008;
321(
5886):.
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.
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