linoleic-acid and Autoimmune-Diseases

Topics: Animals; Autoimmune Diseases; B-Lymphocytes; Dietary Fats; Evaluation Studies as Topic; Fatty Acids, Unsaturated; Guinea Pigs; Humans; Immunocompetence; Infections; Linoleic Acid; Linoleic Acids; Lymphocyte Activation; Mice; Neoplasms; Rats; T-Lymphocytes

Topics: Animals; Autoimmune Diseases; Dietary Fats; Fatty Acids, Essential; Fish Oils; Humans; Kidney Diseases; Linoleic Acid; Linoleic Acids

Topics: Autoimmune Diseases; Autoimmunity; Humans; Linoleic Acid

Topics: Autoimmune Diseases; Humans; Linoleic Acid; Mendelian Randomization Analysis

Topics: Autoimmune Diseases; Humans; Linoleic Acid; Mendelian Randomization Analysis; Polymorphism, Single Nucleotide

Type 1, or cellular, immune response is characterized by overproduction of IL-1, IL-2, IFN-gamma and TNF-alpha and is the underlying immune mechanism of some autoimmune disorders such as psoriasis, alopecia areata, rheumatoid arthritis, Crohn's disease, multiple sclerosis, insulin-dependent diabetes mellitus and experimental autoimmune uveitis. Type 2 immune response is seen in allergic and antibody-mediated autoimmune diseases and is characterized by IL-4, IL-6 and IL-10 overproduction. Linoleic acid is a precursor of prostaglandin E2 (PGE2) and its intake results in tissue production of PGE2, especially in the absence of other polyunsaturated fatty acids (PUFAS) which inhibit this conversion. PGE2 decreases the production of IL-1, IL-2, IFN-gamma and TNF-alpha and proliferation of TH1 cells and increases the production of IL-4, leading to suppression of the type 1 immune response. Taken together, linoleic acid, the major PUFA of maize oil, could have therapeutic efficacy against cellular autoimmune disorders. On the other hand, excessive intake of linoleic acid may aggravate type 2 autoimmune disorders.

Topics: Autoimmune Diseases; Dinoprostone; Humans; Immune System; Linoleic Acid

Essential fatty acid (EFA) deficiency exerts a striking protective effect in several animal models of autoimmune disease. We now report that EFA deprivation prevents diabetes in the BB rat, an animal model of human insulin-dependent diabetes mellitus. In diabetes-prone (DP)-BB rats, the incidences of spontaneous diabetes and insulitis (the pathological substrate of autoimmune diabetes) were greatly reduced by EFA deficiency. This beneficial effect of the deficiency state was also seen in diabetes-resistant (DR)-BB rats that, after treatment with antibody to eliminate RT6+ T cells, would otherwise have become diabetic. The susceptibility of EFA-deprived DP-BB rats to spontaneous diabetes was restored when they were given dietary supplements of linoleate at 70 d of age (during the usual period of susceptibility), but not when they were repleted beginning at 120 d (after the peak incidence of diabetes). EFA deficiency did lead to growth retardation, but calorically restricted control rats demonstrated that the protective effect of the deficiency state was not a function of decreased weight. To examine the relationship between the biochemical changes of EFA deficiency and its physiological effects in this system, we compared the fatty acid changes that occurred in EFA-deficient animals that did and did not develop diabetes. Nondiabetic animals had significantly lower levels of (n-6) fatty acids (i.e., linoleate and arachidonate) and higher levels of oleate, an (n-9) fatty acid, than did diabetic animals. Levels of 20:3(n-9), the fatty acid that uniquely characterizes EFA deficiency, were similar in both groups, however. Among diabetic EFA-deficient rats, the age at onset of diabetes was found to correlate inversely with the level of (n-6) fatty acids, the least depleted animals becoming diabetic earliest, whereas there was no correlation with levels of 20:3(n-9). Among animals repleted with linoleate beginning at 70 d, restoration of susceptibility to diabetes correlated with normalization of the level of arachidonate. In summary, EFA deprivation reduced the frequency of diabetes in both DP and RT6-depleted DR-BB rats. This protective effect was strongly associated with depletion of (n-6) fatty acids, particularly arachidonate, but not with accumulation of the abnormal 20:3(n-9). Conjecturally, arachidonate and/or a metabolite may play a key role in mediating inflammatory injury in this animal model of autoimmune diabetes.

Topics: Animals; Autoimmune Diseases; Body Weight; Diabetes Mellitus, Experimental; Fatty Acids; Fatty Acids, Essential; Female; Linoleic Acid; Linoleic Acids; Macrophages; Male; Rats; Rats, Inbred BB

The MRL/MpJ-lpr/lpr mice manifest a T cell proliferative and autoimmune disorder. Similar changes occur much later in the life of MRL/MpJ-+/+ mice. MRL/MpJ-lpr/lpr (lpr/lpr) and MRL/MpJ-+/+ (+/+) mice were fed for six weeks nutritionally adequate semipurified diets containing 20% (w/w) fat, but differing in linoleic acid content. The phospholipid fatty acid composition of T and B cells was found to be dependent on genetic background of mice and level of linoleic acid in the diet. Changes in the levels of specific fatty acids like 16:0, 18:2 omega 6, 22:5 omega 3 and 22:6 omega 3 in some of the phospholipid components were observed in the MRL/MpJ-lpr/lpr strain in both the B and T cell types as compared with their normal +/+ counterpart strain. T cells of lpr/lpr mice exhibited significantly higher levels of 20:4 omega 6 than did T cells of other strain. High levels of dietary linoleic acid significantly increased incorporation of 18:2 omega 6 in T and B cells, while the effect on other fatty acids of the two types of cells varied with the phospholipid classes and fatty acids when compared with the low linoleic acid fed-group. Differences observed in the phospholipid fatty acid composition of the T and B cells of the congenic mice might contribute to differences in rate of progression of age-related changes suggesting that the autoimmune disorder might be mitigated by dietary manipulation.

Topics: Animals; Autoimmune Diseases; B-Lymphocytes; Dietary Fats, Unsaturated; Fatty Acids; Female; Genotype; Linoleic Acid; Linoleic Acids; Lymphocytes; Mice; Mice, Mutant Strains; Phospholipids; Spleen; T-Lymphocytes

Topics: Abetalipoproteinemia; Adenine Nucleotides; Adenosine Triphosphate; Autoimmune Diseases; Blood Protein Disorders; Celiac Disease; Cholesterol; Congenital Abnormalities; Erythrocytes; Glucosephosphate Dehydrogenase; Hemoglobinometry; Hemolysis; Linoleic Acid; Lipid Metabolism; Lipoproteins; Metabolism; Methemoglobin; Neurologic Manifestations; Osmosis; Phospholipids; Research