The effect of Conjugated Linoleic Acid and its 9:11 and 10:12 isomers on the inflamatory profiles on monocytic / macrophage and endothelial cell systems
University of Wales
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This study investigated the role of the dietary lipid Conjugated Linoleic Acid (CLA) as a 50:50 mixture of 9:11 CLA and 10:12 CLA and these two isoforms used individually, in regulating the carboxymethyllysine (CML) induced inflammatory response in human monocytic, macrophage and endothelial cells. CML is a glycated amadori product that has a crucial role in activating the inflammation in type 2 diabetes (T2D). All three forms of the lipid at non-toxic levels were capable of significantly reducing the release of two inflammatory cytokines (TNF-α and IL-6) in monocytes and macrophages and IL-6 in endothelial cells. In contrast the non-conjugated Linoleic Acid (LA) did not significantly reduce these cytokines in any of the cell types investigated. All isomers were capable of activating both forms of the nuclear transcription factors Peroxisome Proliferator Activated Receptors (PPAR) α and ϒ in monocytes and macrophages. CLA induced significantly the activation in the transcription factor important in regulating the inflammatory response, nuclear factor-kappa B (NF-κB). However, in cells treated with CML, CLA significantly reduced the activation of NF-κB as measured by DNA binding in cells pre-treated with CML-suggesting an ability to trensrepress the activity of NF-κB, possibly in conjunction with the PPARs and supporting an anti-inflammatory role for the lipid in activated cells. All three forms of the lipid were significantly able to regulate expression of the receptor for glycated proteins (RAGE) in monocytes, macrophages and endothelial cells. Gene reporter assays demonstrated that in endothelial cells, that CLA was capable of suppressing the transcriptional activity of promoters which contain promoters for NF-κB response elements, either as part of a recombinant construct or as a cloned fragment of the human RAGE promoter. Hence, in conclusion it would appear that the CLAs investigated in this study could significantly suppress the inflammation in diseases such as T2D through their ability to suppress NF-κB leading to down-regulation of RAGE expression. Furthermore, these events appear to be consistent for all three forms of CLA investigated and in all three cell types-all with a critical role in the development of atherosclerosis.
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