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Publication : Modulation of gene expression via disruption of NF-kappaB signaling by a bacterial small molecule.

First Author  Kravchenko VV Year  2008
Journal  Science Volume  321
Issue  5886 Pages  259-63
PubMed ID  18566250 Mgi Jnum  J:137441
Mgi Id  MGI:3799565 Doi  10.1126/science.1156499
Citation  Kravchenko VV, et al. (2008) Modulation of gene expression via disruption of NF-kappaB signaling by a bacterial small molecule. Science 321(5886):259-63
abstractText  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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