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Essential Fatty Acids and Inflammation

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Essential Fatty Acids and Inflammation Annals ofthe Rheumatic Diseases 1991; 50: 745-746 745 Ann Rheum Dis: first published as 10.1136/ard.50.11.745 on 1 November 1991. Downloaded from Essential fatty acids and inflammation Essential fatty acids are 'essential'" not only because of their deprivation of linoleic acid leads to deficiency of arachidonic physiological importance but because they must be derived acid and impairment of prostaglandin synthesis. Essential in either direct or partially elaborated form from the diet. fatty acid deficiency causes many pathological changes, but Thus these acids may be classified as vitamins (indeed they it also reduces the severity of inflammation in experimental were once called vitamin F). animal models. Fasting also has a salutary effect on Two groups offatty acids are essential to the body: the W6 symptoms of patients with rheumatoid arthritis.3 As neither (n6) series, derived from linoleic acid (18:2 n-6) and the W3 induction of essential fatty acid deficiency nor fasting are (n6) series, derived from a-linolenic acid (18:3 n-3). In these likely to be popular treatments it might be more prudent to notations 18 is the number of carbon atoms in the molecule, modify or supplement, rather than delete, lipid intake. the second number is the number of double carbon-carbon The extraordinary rapidity with which platelets adhere to bonds (degree of unsaturation), and the number after the n damaged tissue, aggregate, and release potent biologically is the position of the first double bond starting from the active materials suggests that the platelet is well suited to be methyl (w) end of the fatty acid chain. The figure shows the a cellular trigger for the inflammatory process.4 Thus efforts sequences of the two fatty acids. Fatty acids provide energy, directed at suppression of thromboxane synthesis, enhance- are an integral part of cell membranes, and are precursors for ment of prostacyclin (prostaglandin I2) production, and prostaglandins, thromboxanes, and leukotrienes, collectively inhibition of platelet aggregation may result in limitation of termed eicosanoids. Abundant experimental evidence inflammatory responses. Fish oil lipids, rich in eicosapen- supports the view that eicosanoids participate in develop- taenoic acid (20:5 n3), inhibit formation of cyclo-oxygenase ment and regulation of immunological and inflammatory products (thromboxane A2, prostaglandin E2) derived from responses. Because most rheumatic diseases are characterised arachidonate. Newly formed throboxane A3 has much less by inflammation, disordered immune regulation, and tissue ability than thromboxane A2 to constrict vessels and aggre- injury there is much interest among rheumatologists in the gate platelets. In addition, production of prostaglandin I2 by role of eicosanoids in regulation of host defences. As the endothelial cells is not reduced appreciably by increased detrimental effects of therapy for the rheumatic diseases eicosapentaenoic acid content, and the physiological activity may be more difficult to manage than the diseases themselves of newly synthesised prostaglandin I3 is added to that of there is a need for new, safe approaches to the treatment of prostaglandin I2.5 Diets enriched in fish oil also reduce the these patients. Alteration of the eicosanoid profile by amount of leukotriene B4 generated via the 5-lipoxygenase administration offatty acid precursors other than arachidonic pathway in stimulated neutrophils and monocytes, suppress acid is one approach under investigation. the chemotactic response of neutrophils to leukotriene B4, As eicosanoids derive from essential fatty acids, dietary and reduce generation of platelet activating factor, inter- manipulation or direct administration of precursor fatty leukin 1, and tumour necrosis factor by stimulated mono- acids has been used to alter the eicosanoid profile. cytes.6 ' Fish oil supplements have therefore been used in http://ard.bmj.com/ Although changes in eicosanoid production owing to attempts to suppress inflammation in experimental models alteration of fatty acid intake form the basis of the current and in patients with rheumatoid arthritis.>'0 Therapeutic hypothesis for the anti-inflammatory effects of this type of benefits have been modest but encouraging. Evidence that treatment, it is likely that the precursor fatty acids fish oil administration enhances collagen induced arthritis in themselves may alter immune responses. Animal and rats and exacerbates vasculitis in autoimmune mice" human studies have shown that changes in essential fatty dictates caution in the premature uncontrolled use of fish oil acid intake alter the fatty acid composition of cell mem- treatments in inflammatory diseases. on September 24, 2021 by guest. Protected copyright. branes.2 For example, in essential fatty acid deficiency, Evidence obtained from experiments in vitro and in vivo in small animals and humans suggests that other novel fatty cp6 (n-6)tatt acids 3aUn3 IM a acids may be safe and effective anti-inflammatory and Linoleic acid a-Linoleric acid immunomodulatory agents. For example, certain botanical (18:2) (18:3) lipids, notably those extracted from seeds of the evening 66 dsaturase II primrose and borage plants, contain relatively large .Unoderic acid 6,9,12,1 5-octadecatetraenoic amounts of y-linolenic acid (18:3 n-6). This acid is (18:3) acid (18:4) converted rapidly to dihomo-y-linolenic acid (20:3 n-6) the Elongase fatty acid precursor of the monoenoic prostaglandins-for PGE Cylo-oxygenase | example, prostaglandin El. In humans the 65 desaturase 1 Dihomo-y- Stearadonic acid (20:4) which converts linolenic acid (20:3) dihomo-y-linolenic acid to arachidonic acid 15-OH DGLA is sluggish. Thus concentrations of arachidonate do not UipoxygenaIse | 65 desaturase II increase appreciably. Dihomo-y-linolenic acid competes Arachidonic acid (20:4) Eicosapentaenoic acid (20:5) with arachidonate for oxidative enzymes, thereby reducing production of cyclo-oxygenase products derived from arachidonate. In addition, dihomo-y-linolenic acid cannot be converted to inflammatory leukotrienes by 5- lipoxygenase. Instead, it is converted to 15-hydroxy- Cydo-oxygenase Lipoxygenase Cydo-oxygenase Lipoxygenase dihomo-y-linolenic acid, which has the added ability of inhibiting 5-lipoxygenase activity.'2 PGI LTB4 PGE, y TxA2 PGE%,TxA3 LTB5 y-Linolenic acid enrichment of diet suppresses acute and chronic inflammation as well Metabolicpathwaysofessentialfattyacids. PGEn=prostaglandinEn; as joint tissue injury in several IS-OHDGLA = 15-hydroxy-dihomo-y-linolenic acid; TxAn =thromboxane experimental animal models.13 In animals treated with An;LTB,-=leukotrieneB,. evening primrose or borage seed oils, cells from inflamma- 746 Zurier Administration of chain tory exudate are enriched in y-linolenic acid and its adverse effects. long poly- Ann Rheum Dis: first published as 10.1136/ard.50.11.745 on 1 November 1991. Downloaded from elongated product dihomo-y-linolenic acid. Exudate prosta- unsaturated fatty acids increases the likelihood of lipid glandin E2 and leukotriene B4 concentrations are reduced peroxidation with its associated toxic effects on cells. It is and leucocyte effector functions (chemotaxis, lysosomal not known whether an increased requirement for an enzyme release) are suppressed. Enrichment with dihomo- antioxidant (such as vitamins E and C) accompanies y-linolenic acid of synovial cells in culture leads to a marked increased intake of long chain unsaturated fatty acids. reduction of prostaglandin E2 synthesis, a substantial Because these novel fatty acids can reduce inflammation and increase in prostaglandin El production, and reduction in affect immunocytes the question arises as to whether they interleukin 1 induced synovial cell proliferation. Addition to can compromise the immune system. Susceptibility to cultures of arachidonic acid (which increases prostaglandin infection has not been seen as yet but must be considered. E2 substantially) or eicosapentaenoic acid does not modify The potential ability of particular fatty acids to regulate synovial cell proliferation. The antiproliferative effect of cell activation, immune responses, and inflammation is dihomo-y-linolenic acid is prevented by indomethacin.'4 exciting to consider at the clinical, cellular, and molecular Thus both marine and botanical lipids have anti-inflamma- levels. A better understanding of how fatty acids modulate tory actions owing to their ability to reduce synthesis of function of cells involved in host defence might lead to oxygenation products of arachidonic acid which are potent development of new, benign treatment for diseases charac- mediators of inflammation. terised by acute and chronic inflammation. In addition to their role as eicosanoid precursors, fatty acids are of major importance in maintaining cell membrane Division ofRheumatology, B ZURIER Department of Medicine, structure and are key determinants of the behaviour of University of Massachusetts Medical Center, membrane bound enzymes and receptors.'5 The fatty acid 55 Lake Avenue North, precursors can exert these functions directly and therefore Worcester, MA 01655, may themselves be important regulators of immune USA responses. Dihomo-y-linolenic acid suppresses interleukin 2 production by human peripheral blood mononuclear cells in vitro, suppresses proliferation of interleukin 2 dependent 1 Burr G 0, Burr M M. On the nature and role of the fatty acids essential in nutrition. J Biol Chem 1930; 86: 587-621. human T lymphocytes, and reduces expression
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