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© 2005 The American Society for Nutritional Sciences J. Nutr. 135:239-244, February 2005


Nutritional Immunology

Conjugated Linoleic Acid Attenuates the Production and Gene Expression of Proinflammatory Cytokines in Weaned Pigs Challenged with Lipopolysaccharide1

Lai Changhua, Yin Jindong, Li Defa2, Zhao Lidan, Qiao Shiyan and Xing Jianjun

College of Animal Science and Technology, China Agricultural University, Beijing, P.R. China

2To whom correspondence should be addressed. E-mail: defali{at}public2.bta.net.cn.

We investigated the anti-inflammatory role of conjugated linoleic acid (CLA) in inflammation-challenged weaned pigs and in in vitro cultured peripheral blood mononuclear cells (PBMCs). To test the hypothesis that inflammation responses can be attenuated by dietary CLA supplementation, we used an acute inflammation model in which pigs were injected with lipopolysaccharide (LPS). After 14 d of dietary supplementation with either 2% soybean oil or 2% CLA, half of the pigs in each diet group were challenged with LPS. Dietary CLA alleviated growth depression and prevented the elevations in production and mRNA expression of proinflammatory cytokines [i.e., interleukin (IL)-6 and tumor necrosis factor (TNF)-{alpha}] induced by the LPS challenge. CLA enhanced the expression of interleukin-10 (IL-10) and peroxisome proliferator-activated receptor-{gamma} (PPAR{gamma}) in spleen and thymus. To further elucidate the inhibitory effects and the mechanism of action of CLA on cytokine profiles (i.e., IL-1ß, IL-6, and TNF-{alpha}), PBMCs were isolated from weaned pigs and cultured in media containing cis-9, trans-11 (9c,11t) CLA and trans-10, cis-12 (10t,12c) CLA. Each CLA isomer suppressed the production and expression of IL-1ß, IL-6, and TNF-{alpha}, and enhanced PPAR{gamma} activation and gene expression in cultured PBMCs. At the molecular level, the inhibitory actions of CLA on IL-1ß, IL-6, and TNF-{alpha} are attributable mainly to 10t,12c-CLA and the anti-inflammatory properties of CLA are mediated, at least in part, through a PPAR{gamma}-dependent mechanism.


KEY WORDS: • proinflammatory cytokine • conjugated linoleic acid • PPAR{gamma} • pigs • growth suppression




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