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. |