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However, IL-6 is the only cytokine benefit that benefit can stimulate the synthesis of all the acute phase proteins involved in the inflammatory benefit response: C-reactive protein, serum amyloid A, fibrinogen, 1-chymotrypsin and haptoglobin [76]. There is evidence that phospholipase A2 and cyclooxygenase pathways of AA metabolism are involved in the action of IL-6 in platelets (aggregation). Khalfoun et al. [77] examined the effects of PUFA on the production of IL-6 by human unstimulated endothelial cells and stimulated endothelial cells with TNF, IL-4, LPS (lipopolysaccharide) or PBL (allogeneic peripheral blood lymphocytes). The addition of EPA and DHA significantly reduced the production of IL-6 whereas AA was ineffective even at highest concentrations. EPA was more potent than DHA. Interleukin-6 occupies a central place in the inflammatory response. Woods et al. [39] suggest a link between IL-6 and cardiovascular disease and the pathways involved (Fig. 2). The discovery of genetic polymorphisms involving a change of a single base, from guanine to cytosine, at position174 in the 5' flanking region of the interleukin-6 gene is of great importance because the G allele is associated with higher IL-6 production than the C allele.
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