Docosahexaenoic acid ingestion inhibits natural killer cell activity and production of inflammatory mediators in young healthy men

Citation
Ds. Kelley et al., Docosahexaenoic acid ingestion inhibits natural killer cell activity and production of inflammatory mediators in young healthy men, LIPIDS, 34(4), 1999, pp. 317-324
Citations number
45
Categorie Soggetti
Agricultural Chemistry","Biochemistry & Biophysics
Journal title
LIPIDS
ISSN journal
00244201 → ACNP
Volume
34
Issue
4
Year of publication
1999
Pages
317 - 324
Database
ISI
SICI code
0024-4201(199904)34:4<317:DAIINK>2.0.ZU;2-S
Abstract
The purpose of this study was to examine the effects of feeding docosahexae noic acid (DHA) as triacylglycerol on the fatty acid composition, eicosanoi d production, and select activities of human peripheral blood mononuclear c ells (PBMNC). A 120-d study with 11 healthy men was conducted at the Metabo lic Research Unit of Western Human Nutrition Reach Center. Four subjects (c ontrol group) were fed the stabilization diet throughout the study; the rem aining seven subjects were fed the basal diet for the first 30 d, followed by 6 g DHA/d for the next 90 d. DHA replaced an equivalent amount of linole ic acid; the two diets were comparable in their total fat and all other nut rients. Both diets were supplemented with 20 mg D alpha-tocopherol acetate per day. PEMNC fatty acid composition and eicosanoid production were examin ed on day 30 and 113; immune cell functions were tested on day 22, 30, 78, 85, 106, and 113. DHA feeding increased its concentration from 2.3 to 7.4 w t% in the PBMNC total lipids, and decreased arachidonic acid concentration from 19.8 to 10.7 wt%. It also lowered prostaglandin E2 (PGE2) and leukotri ene B4 (LTB4) production, in response to lipopolysaccharide, by 60-75%. Nat ural killer cell activity and in vitro secretion of interleukin-1 beta and tumor necrosis factor a were significantly reduced by DHA feeding. These pa rameters remained unchanged in the subjects fed the control diet. B-cell fu nctions as reported here and T-cell functions that we reported previously w ere not altered by DHA feeding. Our results show that inhibitory effects of DHA on immune cell functions Varied with the cell type, and that the inhib itory effects are not mediated through increased production of PGE2 and LTB 4.