Trans-10, cis-12-conjugated linoleic acid attenuates tumor necrosis factor-[alpha] production by lipopolysaccharide-stimulated porcine peripheral blood mononuclear cells through induction of interleukin-10
Conjugated linoleic acid (CLA) can stimulate or inhibit immune cell function, and among CLA isomers, trans-10, cis-12 (t10c12)-CLA was shown to participate in the modulation of pro- or anti-inflammatory cytokine secretion. The objective of this study was to examine the effect of t10c12-CLA on tumor...
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Veröffentlicht in: | Cytokine (Philadelphia, Pa.) Pa.), 2011-11, Vol.56 (2), p.224-230 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Conjugated linoleic acid (CLA) can stimulate or inhibit immune cell function, and among CLA isomers, trans-10, cis-12 (t10c12)-CLA was shown to participate in the modulation of pro- or anti-inflammatory cytokine secretion. The objective of this study was to examine the effect of t10c12-CLA on tumor necrosis factor (TNF)-[alpha] production by lipopolysaccharide (LPS)-stimulated porcine peripheral blood mononuclear cells (PBMCs). In addition, we determined whether these effects were associated with the induction of interleukin (IL)-10. Treatment of LPS-unstimulated porcine PBMCs with t10c12-CLA increased both TNF-[alpha] expression and IL-10 production. However, treatment of LPS-stimulated porcine PBMCs with t10c12-CLA suppressed TNF-[alpha] production and increased the levels of IL-10. Furthermore, treatment of LPS-stimulated porcine PBMCs with IL-10 suppressed the production of TNF-[alpha]. The effects of t10c12-CLA on TNF-[alpha] expression by both LPS-naieve and LPS-stimulated PBMCs were inhibited by IL-10 treatment. The suppressive effects of t10c12-CLA on TNF-[alpha] production by LPS-stimulated porcine PBMCs were inhibited by an anti-IL-10 polyclonal antibody. These findings suggest that t10c12-CLA has an immunostimulatory effect on porcine PBMCs mediated via the up-regulation of TNF-[alpha] production, and an anti-inflammatory effect in LPS-stimulated PBMCs mediated via the down-regulation of TNF-[alpha] production, and that both is likely to be associated with the induction of IL-10. |
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ISSN: | 1043-4666 |
DOI: | 10.1016/j.cyto.2011.06.019 |