Dietary fish oil augments the induction of arthritis in rats immunized with type II collagen.
- 1 February 1984
- journal article
- research article
- Published by The American Association of Immunologists in The Journal of Immunology
- Vol. 132 (2), 725-729
- https://doi.org/10.4049/jimmunol.132.2.725
Abstract
Certain dietary-induced changes in tissue levels of polyunsaturated fatty acids are known to modify inflammatory reactions, possibly through changes in the synthesis of mediators of inflammation derived from fatty acids, including prostaglandins and leukotrienes. We have therefore examined the effects of a fish oil diet, enriched in highly unsaturated (delta-17) long chain fatty acids, on collagen arthritis. Weanling female Sprague-Dawley rats were maintained on a diet with fat provided by either fish oil (containing 14.5% 5, 8, 11, 14, 17-eicosapentaenoic acid; EPA) or, as a control, beef tallow (containing less than 0.05% EPA). They were immunized with native chick type II collagen emulsified in incomplete Freund's adjuvant 5 to 6 wk later. There was an increased incidence of arthritis in the rats receiving the fish oil compared with the group receiving the beef diet (88 vs 61%, p less than 0.001), but there was no significant difference in the severity of joint inflammation of arthritic rats in the two groups. The mean serum titer of IgG antibodies to type II collagen, measured by an enzyme-linked immunosorbent assay (ELISA), was decreased in the group receiving the fish oil (p less than 0.001), whereas the hemagglutinating antibody titer and delayed-type hypersensitivity to collagen were similar in the two groups. Primary synovial explant cultures from fish oil-treated rats produced only 21 to 24% as much PGE2 as beef tallow-treated controls, and this reduction in the experimental group was not accompanied by any detectable increase in PGE3, the E-prostaglandin derived from the arachidonic acid analogue, EPA, in fish oil. These data demonstrate that inductive mechanisms in collagen arthritis can be altered by diet-induced changes in tissue fatty acid composition without essential fatty acid deficiency. The reason(s) for this effect is unknown, but it is possible that changes in the cyclooxygenase or lipoxygenase products of polyunsaturated fatty acids are involved.This publication has 1 reference indexed in Scilit:
- Prevention of Glomerulonephritis and Prolonged Survival in New Zealand Black/New Zealand White F1 Hybrid Mice Fed an Essential Fatty Acid-deficient DietJournal of Clinical Investigation, 1981