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The  Pseudomonas aeruginosa  quorum sensing signal molecule  N -3-oxododecanoyl- l -homoserine lactone (3OC 12 HSL) can inhibit function of the mammalian anti-inflammatory transcription factor peroxisome proliferator activated receptor (PPAR)γ, and can be degraded by human paraoxonase (PON)2. Because 3OC 12 HSL is detected in lungs of cystic fibrosis (CF) patients infected with  P. aeruginosa,  we investigated the relationship between  P. aeruginosa  infection and gene expression of PPARγ and PON2 in bronchoalveolar lavage fluid (BALF) of children with CF. Total RNA was extracted from cell pellets of BALF from 43 children aged 6 months–5 years and analyzed by reverse transcription–quantitative real time PCR for gene expression of PPARγ, PON2, and  P. aeruginosa lasI,  the 3OC 12 HSL synthase. Patients with culture-confirmed  P. aeruginosa  infection had significantly lower gene expression of PPARγ and PON2 than patients without  P. aeruginosa  infection. All samples that were culture-positive for  P. aeruginosa  were also positive for  lasI  expression. There was no significant difference in PPARγ or PON2 expression between patients without culture-detectable infection and those with non-Pseudomonal bacterial infection, so reduced expression was specifically associated with  P. aeruginosa  infection. Expression of both PPARγ and PON2 was inversely correlated with neutrophil counts in BALF, but showed no correlation with other variables evaluated. Thus, lower PPARγ and PON2 gene expression in the BALF of children with CF is associated specifically with  P. aeruginosa  infection and neutrophilia. We cannot differentiate whether this is a cause or the effect of  P. aeruginosa  infection, but propose that the level of expression of these genes may be a marker for susceptibility to early acquisition of  P. aeruginosa  in children with CF.

Expression of PPARγ and Paraoxonase 2 Correlated with Pseudomonas aeruginosa Infection in Cystic Fibrosis