Date of Award

Spring 5-12-2017

Document Type

Thesis

Degree Name

Master of Biological Science (MBioSci)

Department

Biology

First Advisor

Dr. Virginia Rider

Second Advisor

Dr. Dixie L. Smith

Third Advisor

Dr. Pawan Kahol

Abstract

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 a 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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