Lípidos e imunidade
Keywords:
Inflammation, infection, polyunsaturated fatty acids, eicosanoids, atherosclerosisAbstract
Epidemiologic data suggest a link between
atherosclerosis and chronic infections and inflammatory conditions. During infection and
inflammation, a wide range of alterations in metabolism occur. These are part of the body´s reaction known as the acute phase response (APR). Infection and inflammation can also perturb lipoprotein metabolism and produce a wide
variety of changes in the plasma concentrations of lipids and lipoproteins.
Eicosanoids are a group of oxygenated fatty
acids with diverse and potent biological activity, produced from the fatty acids. The variety
of eicosanoids products and their correspondingly diverse physiological effects have been well characterized, and probably represent the best-understood relationship between lipids and biological function. Consequently, attempts to
modulate the production of eicosanoids must
target either the enzyme activities responsible for synthesizing eicosanoids or the concentration of fatty acids substrate entering biological system through the diet.
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References
Robinson D, Section 2, Evaluation, signs and symptoms-Inflamation. In : Klippel J, Dieppe P, Rheumatology, Mosby, London Edinburgh,
New York, Philadelphia, St Louis, Sydney, Toronto, 2000, 1.1.1-1.11.8
German J, Dillard C, Whelan J. Biological effects of dietary arachidonic acid. J. Nutrition 1995; 126:1076S-1080S.
Watkins S, German J, shoenfeld Y Gershwin M. II Pathogenic Immune Mechanism of Atherosclerosis – Lipids and Immunity. In: Shoenfeld Y, Harats D, Wick G. Atherosclerosis and Autoimmunity. Elsevier Amsterdam, Lausanne, New York, Oxford, Shannon, Singapore,
Tokyo.2001;29-114
Khovidhunkit W, Memon R, Feingold K et al. Infection and inflammation-induced proatherogenic changes of lipoproteins. The Journal
of Infectious Diseases. 2000;181 ( Suppl 3 ): S462-72
Ilowite N. Hyperlipidemia and the rheumatic diseases. Current Opinion in Rheumatology. 1996; 8:455-458.
Ilowite N. Premature atherosclerosis in systemic lupus erythematosus. J Rheumatol 2000; 27:Suppl 58: 15-19
Bruce I, Urowitz M, Gladman D, et al. Natural history of hypercholesterolemia in systemic lupus erythematosus. J Rheumatol 1999;26:2137-
Bruce I, Gladman D, Urowitz M. Detection and modification of risk factors for coronary artery disease in patients with systemic lupus
erythematosus: A quality improvement study.Clinical and Experimental Rheumatology 1998; 16:435-440.
Hellerstein M, Grunfeld C, Wu K et al. Increased de novo hepatic lipogenesis in human immunodeficiency virus infection. J Clin Endocrinol Metab 1993; 76:559-565.
Walzem R, Watkins S, Frankel E, et al. Older plasma lipoproteins are more susceptible to oxidation: A linking mechanism for the lipid and
oxidation theories of atherosclerotic cardiovascular disease. Proc. Natl. Acad. Sci. USA 1995; 92: 7460-7464.
Chait A, Brazg R, Tribble D, et al. Susceptibility of small, dense, low-density lipoproteins to oxidative modification in subjects with the atherogenic lipoprotein phenotype, pattern B. The American Journal of Medicine 1993;94: 350-356
Memon A, Staprans I, Noor M, et al. Infection and inflammation induce LDL Oxidation in vivo. Arteriosclerosis, Thrombosis and Vascular
Biology 2000;20 (6):1536-1542
Marathe S, Schissel S, Yellini M, et al. Human vascular endothelial cells are a rich and regulatable source of scretory sphingomyelinase.
The Journal of Biological Chemistry 1998; 273 (7): 4081-4088
Memon R, Holleran M, Moser H,et al. Endotoxin and cytokines increase hepatic sphingolipid biosynthesis and produce lipoproteins enriched in ceramides and sphingomyelin. Arteriosclerosis, Thrombosisand Vascular Biology 1998; 18 (8): 1257-1265
Schissel S, Jiang X, Tweedl-Hardman J, et al. Secretory sphingomyelinase gene, can hydrolyse atherogenic lipoproteins at neutral ph. The
Journal of Biological Chemistry 1998; 273 (5): 2738-2746
Schissel S, Keesler G, Schuchman E, et al. The cellular trafficking and zinc dependence of secretory and lysosomal sphingomyelinase, two
products of acid sphingomyelinase gene. The Journal of Biological Chemistry 1998;273 (29);18250-18259
Schissel S, Schuchman E, Williams K, et al. Zn2+ stimulated sphingomyelinase is secreted by many cell types and is a product of the
acid sphingomyelinase gene. The Journal of Biological Chemistry1996; 271 (31): 18431-18436
Goldkorn T, George J, Lavrentiadou S, et al. II Pathogenic Immune Mechanism of Atherosclerosis – Ceramide pathway and apoptosis in
autoimmunity and atherosclerosis. In: Shoenfeld Y, Harats D, Wick G. Atherosclerosis and Autoimmunity. Elsevier Amsterdam, Lausanne, New York, Oxford, Shannon, Singapore, Tokyo. 2001;29-114
Schissel S, Tweedl-Hardman J, Rapp J, et al. Rabbit aorta and human atherosclerotic lesions hydrolize the sphingomyelin of retained low-density lipoprotein. J. Clin. Invest.1996; 98(6):1455-1464
Borba E, Bonfa E, Vinagre C, et al.Chylomicron metabolism is markedly altered in systemic lupus erythematosus. Arthritis & Rheumatism 2000; 43 (5):1033-1040
Ly H, Francone O, Fielding C, et al. Endotoxin and TNF lead to reduced plasma LCAT activity and decreased hepatic LCAT mRNA levels
in Syrian hamsters. Journal of Lipid Research 1995; 36:1254-1263
Hardardóttir I, Moser A, Fuller J, et al. Endotoxin and cytokines decrease serum levels and extra hepatic protein and mRNA levels of
cholesteryl ester protein in Syrian hamsters. The Journal of ClinicalInvestigation 1996; 97(11): 2585-2592
Lamping N, Dettmer R, Schroder N, et al. LPS-binding protein mice from septic shock caused by LPS or Gram-negative bacteria. J. Clin.
Invest.1998; 101(10): 2065-2071
Grunfeld C, Marshall M, Shigenaga J, et al. Lipoproteins inhibit macrophage activation by lipoteichoic acid. Journal of Lipid Research
; 40: 245-252
Feingold K, Hardardottir I, Memon R, et al. Effect of endotoxin on cholesterol biosynthesis and distribution in serum lipoprotein in Syrian hamsters. Journal of Lipid Research 1993; 34: 2147-2158
Simopoulos A. Essential fatty acids in healyh and chronic disease. Am J Clin Nutr 1999; 70(suppl): 560S-569S
Woods K, Thien K, Abramson J. Dietary marine fatty acids (fish oil) for asthma. The cochrane database of systemic reviews. The Cochrane
Library, Copyright 2001; Volume (Issue 3) (no page)
Linos A, Kaklamani V, Kaklamani E, et al. Dietary factors in relation to rheumatoid arthritis: a role for olive oil and cooked vegetables? Am
J Clin Nutr 1999; 70:1077-1082
Hall A, Parbtani A, Clark W, et al. Abrogation of MRL/Ipr lupus nephritis by dietary flaxseed. American Journal of Kidney Diseases 1993;
(2):326-332
Clark W, Parbtani A, Huff M, et al. Flaxseed : A potential treatment for lupus nephritis. Kidney International 1995; 48:475-480
Belch J, Hill A. Evening primrose oil and borage oil in rheumatoid conditions. Am J Clin Nutr 2000; 71 (suppl): 352S-356S
Kremer J, Lawrence D, Jubiz W, et al. Dietary fish oil and olive oil supplementation in patients with rheumatoid arthritis. Arthritis and
Rheumatism 1999; 33(6):810-820
James M, Gibson R, Cleland L. Dietary polyunsaturated fatty acids and inflammatory mediator production. Am J Clin Nutr 2000; 71(suppl): 343S-348S
Lauritsen K, Laursen L, Bukhave K. Use of colonic eicosanoid concentration as predictors of relapse in ulcerative colitis: double blind
placebo controlled study on sulphalazine maintenance treatment. Gut1988; 29: 1316-1321
Esteve M, Navarro E, Klasseen J, et al. Plasma and mucosal fatty acid pattern in colectomized ulcerative colitis patients. Digestive Diseases
and Sciences 1998; 43(5):1071-1078
Arend W, Dayer J. Inhibition of the production and effects of interleukin-1 and tumor necrosis factor a in rheumatoid arthritis. Arthritis and Rheumatism 1995; 38(2): 151-160
Caughey G, Mantzioris E, Gibson R, et al. The effect on human tumor necrosis factor a and interleukin 1b production of diets enriched in n.3 fatty acids from vegetable oil or fish oil. Am J Clin Nutr 1996; 63:116-122
Endres S, Ghorbani R, Kelley V, et al. The effect of dietary supplementation with n-3 polyunsaturated fatty acids on the synthesis of interleukin-1 and tumor necrosis factor by mononuclear cells. The New England Journal of Medicine 1989; 320 (5):265-271
Hughes D, Pinder A. n-3 Polyunsaturated fatty acids inhibit the antigen-presenting function of human monocytes. Am J Clin Nutr 2000;
(suppl):357S-360S
Hughes D, Southon S, Pinder A. (n-3) Polyunsaturated fatty acids modulate the expression of functionally associated molecules on human monocytes in vitro. J. Nutr. 1996; 126:603-610
Fernandes G, Bysani C, Venkatraman J. Increased TGF-b and decreased oncogene expression by w-3 fatty acids in the spleen delays onset
of autoimmune disease in B/W mice. Journal of Immunology 1994;152:5979-5987
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