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Long-chain polyunsaturated fatty acids (n-3 LC-PUFAs) show beneficial treatment effects on chronic inflammatory diseases of the lung, however, the underlying molecular mechanisms are not well understood. I hypothesize that changes in the regulation of pro-inflammatory cytokines, chemokines and I-CAM cell adhesion molecules are central to bacterial lung infections. To test this hypothesis, I investigated the effect of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) on pro-inflammatory cytokines, chemokines, and I-CAM expression. NL-20 lung epithelial cell lines were treated with 3 mM fatty acid without and with addition of a virulent strain of Streptococcus pneumonia (~1.5 x 108 CFU/ml) for 18 h. Real-time PCR using Taqman assays was employed to determine changes in gene expression in response to treatments. Results indicated that LC-PUFAs have distinct effects on the expression of cytokine, chemokine and cell adhesion molecules that contribute to lung inflammation. DHA treatment decreased the expression of interleukin (IL)-1β and TNF-alpha cytokines and increased IL-8 and IL-6 cytokines relative to uninfected cells. EPA appeared more effective in decreasing IL-6, IL-8 while it had minimum effects in decreasing IL-1β and TNF-alpha cytokines expression. Additionally, I-CAM expression was also downregulated by both fatty acids compared to untreated infected cells. The data were analyzed for significant differences by two-way ANOVA. The result showed significant role (P ≤ 0.05) of DHA and EPA in reducing Streptococcus pneumonia infection in human epithelial lung tissue by altering and reducing the gene expression of pro-inflammatory cytokines, chemokines, and cell adhesion molecules.

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