Studies in humans and murine disease models have clearly shown dietary fish oil to possess anti‐inflammatory properties, apparently mediated by the n‐3 polyunsaturated fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). To determine the mechanisms by which dietary EPA and DHA modulate mouse T‐cell activation, female C57BL/6 mice were fed diets containing either 2% safflower oil (SAF), 2% fish oil (FO), or a 2% purified EPA/DHA ethyl ester mixture for 14 days. Splenic CD4 T cells (∼90% purity) or CD8 T cells (∼85% purity) were incubated with agonists which act at the plasma membrane receptor level (anti(α)‐CD3/anti(α)‐CD28), the intracellular level (PMA/Ionomycin), or at both the receptor and intracellular levels (αCD3/PMA). CD4 T cells stimulated with αCD3/αCD28 or PMA/Ionomycin proliferated and produced principally IL‐2 (i.e. a Th1 phenotype), whereas the proliferation of CD4 T cells stimulated with αCD3/PMA was apparently driven principally by IL‐4 (i.e. a Th2 phenotype). The IL‐4 driven proliferation of putative Th2 CD4 cells was enhanced by dietary n‐3 fatty acids (P = 0·02). Conversely, IL‐2 production by αCD3/α CD28‐stimulated CD4 T cells was reduced in FO‐fed animals (P < 0·0001). The αCD3/αCD28‐stimulated CD8 cells cultured from FO‐fed animals exhibited a significant decrease (P < 0·05) in proliferation. There were no dietary effects seen in αCD3/PMA‐stimulated CD8 cells, which produced both IL‐2 and IL‐4, or in PMA/Ionomycin‐stimulated CD8 cells, which produced principally IL‐2. These data suggest that dietary n‐3 fatty acids down‐regulated IL‐2 driven CD4 and CD8 activation, while up‐regulating the activation of the Th2 CD4 T‐cell subset. Thus, the anti‐inflammatory effects of n‐3 fatty acids may result in both the direct suppression of IL‐2‐induced Th1 cell activation and the indirect suppression of Th1 cells by the enhanced cross‐regulatory function of Th2 cells.
Clinical & Experimental Immunology – Wiley
Published: Sep 1, 2001
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