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.