In:
Science, American Association for the Advancement of Science (AAAS), Vol. 321, No. 5886 ( 2008-07-11), p. 259-263
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.
Type of Medium:
Online Resource
ISSN:
0036-8075
,
1095-9203
DOI:
10.1126/science.1156499
Language:
English
Publisher:
American Association for the Advancement of Science (AAAS)
Publication Date:
2008
detail.hit.zdb_id:
128410-1
detail.hit.zdb_id:
2066996-3
detail.hit.zdb_id:
2060783-0
SSG:
11
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