The bacterial N-3-oxo-dodecanoyl homoserine lactone (C12) selectively impairs the regulation of NF-κ-B functions in activated mammalian cells, according to the data of a research group from The Scripps Research Institute (USA). The nuclear transcription factor NF-κ-B is indispensable for the defence of the body against invading microbial pathogens. Activation of NF-κ-B controls the innate immune response, thus eradicating harmful pathogens.

If NF-κ-B is impaired by C12, NF-κ-B-controlled genes that encode inflammatory cytokines and other immune regulators are suppressed. This seems to be a strategy of C12-producing pathogens like Pseudomonas aeruginosa to decrease the effect of the innate immune system on them. By this mechanism they can establish and retain long-lasting local infections in mammals, like cystic fibrosis.

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