The type of dietary fat affects the severity of autoimmune disease in NZB/NZW mice.
The type of dietary fat dramatically affects the onset of autoimmune disease in lupus-prone female New Zealand Black/New Zealand White F1 (B/W) mice. Disease development was strikingly slowed in mice fed a diet containing quantities of omega-3 fatty acids (fish oil, FO). By 10 months of age, 94% of the FO mice were still living, whereas all the mice fed a saturated fat diet (lard,L) were dead. Those mice fed a corn oil (CO) diet were intermediate with 35% alive at the 10-month time evaluation. Long after the L and CO groups had succumbed to glomerulonephritis, the FO group had negligible proteinuria. Both B and T cell function, particularly antibody production and resultant circulating immune complex (CIC) levels, were modified by the type of dietary fat. FO mice exhibited lower levels of anti-ds-DNA and lower levels of CICs than L or CO mice. B/W antibody response to a T-independent antigen (DNP-dextran) was enhanced at 8 months of age in FO mice, whereas it was suppressed in L mice. T-dependent (sheep red blood cell) responses at that time period were reduced in all the diet groups, a reflection of the reduced numbers of accessory T cells as determined by FACS analysis. The natural killer (NK) response to YAC-1 cells decreased in the L group from 5 to 9 months of age but remained unchanged in the CO and FO groups. Severe glomerulonephritis was the most common histopathologic finding in the L and CO groups. Arteritis was found in the spleens of nearly all the L and CO mice. Arteritis of the heart, colon and intestine, stomach, kidney, and liver were also seen principally in the L mice. In contrast, most FO mice had minimal to mild glomerulonephritis and no or minimal arteritis in the spleen. It is likely omega-3 fatty acids of fish oil reduce immune-complex-induced glomerulonephritis through production of prostaglandin metabolites with attenuated activity and/or through altering cell membrane structure and fluidity, which may, in turn, affect the responsiveness of immune cells.
D000818:Animals; D000917:Antibody Formation; D000936:Antigen-Antibody Complex / Q000032:analysis; D000950:Antigens, Ly / Q000032:analysis; D001323:Autoantibodies / Q000032:analysis; D001327:Autoimmune Diseases / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D004247:DNA / Q000276:immunology; D004041:Dietary Fats / Q000009:adverse effects*; D005227:Fatty Acids / Q000097:blood; D005260:Female; D005399:Fishes; D006400:Hematocrit; D007113:Immunity, Innate; D007074:Immunoglobulin G / Q000032:analysis; D007694:Killer Cells, Natural / Q000276:immunology; D008055:Lipids / Q000097:blood; D008180:Lupus Erythematosus, Systemic / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D008563:Membrane Lipids / Q000097:blood; D051379:Mice; D008814:Mice, Inbred NZB; D008817:Mice, Mutant Strains; D009821:Oils; D011507:Proteinuria / Q000209:etiology
D000936:Antigen-Antibody Complex; D000950:Antigens, Ly; D001323:Autoantibodies; D004041:Dietary Fats; D005227:Fatty Acids; D007074:Immunoglobulin G; D008055:Lipids; D008563:Membrane Lipids; D009821:Oils; D004247:DNA