Modulation of Gene Expression via Disruption of NF-κB Signaling by a Bacterial Small Molecule

+ See all authors and affiliations

Science  11 Jul 2008:
Vol. 321, Issue 5886, pp. 259-263
DOI: 10.1126/science.1156499

You are currently viewing the abstract.

View Full Text


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.

    View Full Text

    Related Content