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American Journal of Clinical Nutrition, Vol. 87, No. 4, 939-948, April 2008
© 2008 American Society for Nutrition

ORIGINAL RESEARCH COMMUNICATION

Comparison of cytokine modulation by natural peroxisome proliferator–activated receptor {gamma} ligands with synthetic ligands in intestinal-like Caco-2 cells and human dendritic cells—potential for dietary modulation of peroxisome proliferator–activated receptor {gamma} in intestinal inflammation 1,2,3

Rachel Marion-Letellier, Matt Butler, Pierre Déchelotte, Raymond J Playford and Subrata Ghosh

1 From the Gastroenterology Section, Imperial College Faculty of Medicine, Hammersmith Hospital Campus, London, United Kingdom (RM-L, MB, RJP, and SG), and Appareil Digestif Environnement Nutrition, Faculté de Médecine-Pharmacie, Institut Fédératif de Recherches Multidisciplinaires sur les Peptides, Gambetta, France (PD)

Background: Peroxisome proliferator–activated receptor {gamma} (PPAR{gamma}) plays a role in the regulation of intestinal inflammation and is activated by both natural (polyunsaturated fatty acid; PUFAs) and synthetic (troglitazone) ligands. The fatty acid content of defined formula diets may play a role in mediating the antiinflammatory effect, but the mechanism is unclear.

Objective: We evaluated to what extent the effect of PUFAs on intestinal inflammation is mediated via PPAR{gamma}.

Design: The human enterocyte-like cell line Caco-2 and human dendritic cells were stimulated by interleukin (IL) 1β and lipoprotein polysaccharide, respectively, in the presence of PPAR{gamma} agonists (troglitazone or PUFAs) or antagonist (GW9662). Five PUFAs were tested: {alpha}-linolenic acid (ALA), conjugated linoleic acid (CLA), docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), and {gamma}-linolenic acid (GLA). Cytokine production was measured by enzyme-linked immunosorbent assay and PPAR{gamma}, I-{kappa}B, and inducible nitric oxide synthase (iNOS) expression by Western blot.

Results: In Caco-2 cells, IL-6 secretion was significantly decreased by troglitazone, DHA, EPA, and GLA. IL-8 production was significantly decreased by troglitazone, ALA, DHA, EPA, and GLA. PPAR{gamma} expression was significantly increased by troglitazone, DHA, and EPA. iNOS expression was significantly decreased by troglitazone, DHA, and EPA. Troglitazone and PUFAs at 0.1 µmol/L tended to increase the expression of I-{kappa}B. Addition of GW9662 reversed the effect of troglitazone and PUFAs at 0.1 µmol/L on IL-8 production and decreased the expression of PPAR{gamma}. EPA and DHA also modulated the dendritic cell response to lipoprotein polysaccharide.

Conclusions: The tested PUFAs exerted an antiinflammatory effect in vitro in both models. This effect of PUFAs in Caco-2 cells is similar to that of troglitazone on intestinal inflammation mediated by PPAR{gamma}, and the potency of the antiinflammatory effect is linked to the number of double bonds.






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