Dietary Juniperis virginiensis seed oil decreased pentobarbital-associated mortalities among DBA/1 mice treated with collagen-adjuvant emulsions.
The propensity of the fatty acid 5,11,14-eicosatrienoic acid (5,11,14-ETA) to replace arachidonic acid in cell membranes, and its inability to be converted to bioactive eicosanoids, suggest that it may be useful in the treatment of autoimmune disorders. Previously, dietary application of oils extracted from 5,11,14-ETA-rich Platycladus orientalis delayed the onset of autoimmune disease in New Zealand Black mice. To gain more knowledge of the efficacy of this fatty acid toward alleviating immunological disorders, a similar oil was used to examine its effects on collagen-induced arthritis in DBA/1 mice, a model characterized by synovial proliferation and joint infiltration by inflammatory cells. Mice were fed AIN76A diet supplemented with 4% (w/w) of either an oil extracted from the seeds of Juniperis virginiensis (0.4% 5,11,14-ETA); a control oil consisting of equal parts olive, linseed and safflower oils; fish oil (90% fish oil and 10% safflower oil); or safflower oil. Mice were immunized with three injections of collagen-adjuvant emulsions, the first injection was intradermal, and the two subsequent injections were intraperitoneal. Mortalities were recorded following a secondary pentobarbital administration intraperitoneally. Mice from the J. virginiensis group had the lowest mortalities (25%) while safflower oil-fed mice had the highest (59%; p < 0.05). While the J. virginiensis group had the lowest mean CD4/CD8 T lymphocyte ratio, the fish oil group had the highest. These observations suggest that manipulation of eicosanoid production by different dietary lipids had different effects on immune responses, possibly through alterations in T lymphocyte subsets. Hypothetically, a downregulation of prostaglandin E2 release could increase the ratio of T helper 1 to T helper 2 lymphocytes and thereby modulate anaphylactic responses. Also, lowered pro-oxidant status may decrease CD4/CD8 T cell ratios and modify immune function.
Yoshida
S H
SH
Department of Food Science and Technology, University of California, Davis 95616-859, USA.
Siu
J
J
Griffey
S M
SM
German
J B
JB
Gershwin
M E
ME
D000818:Animals; D001169:Arthritis, Experimental / Q000139:chemically induced / Q000188:drug therapy / Q000276:immunology*; D016516:CD4-CD8 Ratio; D003094:Collagen; D004042:Dietary Fats, Unsaturated / Q000008:administration & dosage / Q000627:therapeutic use; D006801:Humans; D007223:Infant; D008297:Male; D051379:Mice; D008811:Mice, Inbred DBA; D010424:Pentobarbital / Q000506:poisoning*; D010938:Plant Oils / Q000008:administration & dosage / Q000627:therapeutic use*; D011041:Poisoning / Q000188:drug therapy*; D012639:Seeds / Q000187:drug effects*; D013154:Spleen / Q000166:cytology; D013929:Thromboxane B2 / Q000097:blood
D004042:Dietary Fats, Unsaturated; D010938:Plant Oils; D013929:Thromboxane B2; D003094:Collagen; D010424:Pentobarbital