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<p>Abstract</p> <p>Background</p> <p>Mucin hypersecretion and mucus plugging in the airways are characteristic features of chronic respiratory diseases like cystic fibrosis (CF) and contribute to morbidity and mortality. In CF, <it>Pseudomonas aeruginosa </it>superinfections in the lung exacerbate inflammation and alter mucus properties. There is increasing evidence that n-3 polyunsaturated fatty acids (PUFAs) exhibit anti-inflammatory properties in many inflammatory diseases while n-6 PUFA arachidonic acid (AA) favors inflammatory mediators such as eicosanoids prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) that may enhance inflammatory reactions. This suggests that n-3 PUFAs may have a protective effect against mucus over-production in airway diseases. Therefore, we hypothesized that n-3 PUFAs may downregulate mucins expression.</p> <p>Methods</p> <p>We designed an absolute real-time PCR assay to assess the effect of a 5-week diet enriched either with n-3 or n-6 PUFAs on the expression of large mucins in the lungs of mice infected by <it>P. aeruginosa</it>.</p> <p>Results</p> <p>Dietary fatty acids did not influence mucin gene expression in healthy mice. Lung infection induced an increase of the secreted gel-forming mucin <it>Muc5b </it>and a decrease of the membrane bound mucin <it>Muc4</it>. These deregulations are modulated by dietary fatty acids with a suppressive effect of n-3 PUFAs on mucin (increase of <it>Muc5b </it>from 19-fold up to 3.6 × 10⁵-fold for the n-3 PUFAs treated group and the control groups, respectively, 4 days post-infection and decrease of <it>Muc4 </it>from 15-fold up to 3.2 × 10⁴-fold for the control and the n-3 PUFAs treated groups, respectively, 4 days post-infection).</p> <p>Conclusion</p> <p>Our data suggest that n-3 PUFAs enriched diet represents an inexpensive strategy to prevent or treat mucin overproduction in pulmonary bacterial colonization.</p>