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      Omega-3 Polyunsaturated Fatty Acids for the Treatment of IgA Nephropathy

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      Publication date (Electronic):
      Journal: Journal of Clinical Medicine
      Publisher: MDPI
      Keywords: ω-3 PUFAs, EPA, DHA, IgA nephropathy, aspirin

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          Abstract

          IgA nephropathy is a common disease that causes end-stage renal failure and requires renal replacement therapy. The main purpose of therapeutic intervention in this disease is not limited to improvement of prognosis and prevention of transition to end-stage renal failure, but also prevention of the occurrence of cardiovascular lesions, which increases risk in patients with chronic kidney disease. Steroids and immunosuppressants have been widely used as remission induction therapies; however, the balance between their therapeutic benefits and detrimental side-effects are controversial. In this regard, it is critical to identify alternative therapies which would provide holistic life-long benefits. Currently, the potential of ω-3 fatty acids as anti-inflammatory and inflammation-convergent drugs—especially the remarkable progress of the multifunctional ω-3 polyunsaturated fatty acids (PUFAs)—has garnered attention. In this section, we outline the background and current status of ω-3 PUFA-based treatment in IgA nephropathy.

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          Novel Functional Sets of Lipid-Derived Mediators with Antiinflammatory Actions Generated from Omega-3 Fatty Acids via Cyclooxygenase 2–Nonsteroidal Antiinflammatory Drugs and Transcellular Processing

          Charles Serhan, Clary Clish, Jessica Brannon … (2000)
          Aspirin therapy inhibits prostaglandin biosynthesis without directly acting on lipoxygenases, yet via acetylation of cyclooxygenase 2 (COX-2) it leads to bioactive lipoxins (LXs) epimeric at carbon 15 (15-epi-LX, also termed aspirin-triggered LX [ATL]). Here, we report that inflammatory exudates from mice treated with ω-3 polyunsaturated fatty acid and aspirin (ASA) generate a novel array of bioactive lipid signals. Human endothelial cells with upregulated COX-2 treated with ASA converted C20:5 ω-3 to 18R-hydroxyeicosapentaenoic acid (HEPE) and 15R-HEPE. Each was used by polymorphonuclear leukocytes to generate separate classes of novel trihydroxy-containing mediators, including 5-series 15R-LX5 and 5,12,18R-triHEPE. These new compounds proved to be potent inhibitors of human polymorphonuclear leukocyte transendothelial migration and infiltration in vivo (ATL analogue > 5,12,18R-triHEPE > 18R-HEPE). Acetaminophen and indomethacin also permitted 18R-HEPE and 15R-HEPE generation with recombinant COX-2 as well as ω-5 and ω-9 oxygenations of other fatty acids that act on hematologic cells. These findings establish new transcellular routes for producing arrays of bioactive lipid mediators via COX-2–nonsteroidal antiinflammatory drug–dependent oxygenations and cell–cell interactions that impact microinflammation. The generation of these and related compounds provides a novel mechanism(s) for the therapeutic benefits of ω-3 dietary supplementation, which may be important in inflammation, neoplasia, and vascular diseases.
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            Maresins: novel macrophage mediators with potent antiinflammatory and proresolving actions

            Charles Serhan, Rong Yang, Kimberly Martinod … (2009)
            The endogenous cellular and molecular mechanisms that control acute inflammation and its resolution are of wide interest. Using self-resolving inflammatory exudates and lipidomics, we have identified a new pathway involving biosynthesis of potent antiinflammatory and proresolving mediators from the essential fatty acid docosahexaenoic acid (DHA) by macrophages (MΦs). During the resolution of mouse peritonitis, exudates accumulated both 17-hydroxydocosahexaenoic acid, a known marker of 17S-D series resolvin (Rv) and protectin biosynthesis, and 14S-hydroxydocosa-4Z,7Z,10Z,12E,16Z,19Z-hexaenoic acid from endogenous DHA. Addition of either DHA or 14S-hydroperoxydocosa-4Z,7Z,10Z,12E,16Z,19Z-hexaenoic acid to activated MΦs converted these substrates to novel dihydroxy-containing products that possessed potent antiinflammatory and proresolving activity with a potency similar to resolvin E1, 5S,12R,18R-trihydroxyeicosa-6Z,8E,10E,14Z,16E-pentaenoic acid, and protectin D1, 10R,17S-dihydroxydocosa-4Z,7Z,11E,13E,15Z,19Z-hexaenoic acid. Stable isotope incorporation, intermediate trapping, and characterization of physical and biological properties of the products demonstrated a novel 14-lipoxygenase pathway, generating bioactive 7,14-dihydroxydocosa-4Z,8,10,12,16Z,19Z-hexaenoic acid, coined MΦ mediator in resolving inflammation (maresin), which enhances resolution. These findings suggest that maresins and this new metabolome may be involved in some of the beneficial actions of DHA and MΦs in tissue homeostasis, inflammation resolution, wound healing, and host defense.
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              Omega-3 fatty acids prevent inflammation and metabolic disorder through inhibition of NLRP3 inflammasome activation.

              Yiqing Yan, Wei Jiang, Thibaud Spinetti … (2013)
              Omega-3 fatty acids (ω-3 FAs) have potential anti-inflammatory activity in a variety of inflammatory human diseases, but the mechanisms remain poorly understood. Here we show that stimulation of macrophages with ω-3 FAs, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and other family members, abolished NLRP3 inflammasome activation and inhibited subsequent caspase-1 activation and IL-1β secretion. In addition, G protein-coupled receptor 120 (GPR120) and GPR40 and their downstream scaffold protein β-arrestin-2 were shown to be involved in inflammasome inhibition induced by ω-3 FAs. Importantly, ω-3 FAs also prevented NLRP3 inflammasome-dependent inflammation and metabolic disorder in a high-fat-diet-induced type 2 diabetes model. Our results reveal a mechanism through which ω-3 FAs repress inflammation and prevent inflammation-driven diseases and suggest the potential clinical use of ω-3 FAs in gout, autoinflammatory syndromes, or other NLRP3 inflammasome-driven inflammatory diseases. Copyright © 2013 Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                Fiorella Gurrieri: Role: Academic Editor
                Eugenio Sangiorgi: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): J Clin Med
                Journal ID (iso-abbrev): J Clin Med
                Journal ID (publisher-id): jcm
                Title: Journal of Clinical Medicine
                Publisher: MDPI
                ISSN (Electronic): 2077-0383
                Publication date (Electronic): 19 July 2017
                Publication date Collection: July 2017
                Volume: 6
                Issue: 7
                Electronic Location Identifier: 70
                Affiliations
                Apheresis and Dialysis Center, Keio Univerisity School of Medicine, Tokyo 1608582, Japan; jhira@ 123456keio.jp
                Article
                Publisher ID: jcm-06-00070
                DOI: 10.3390/jcm6070070
                PMC ID: 5532578
                PubMed ID: 28753924
                SO-VID: cd103d7b-89ae-4750-a497-2ee59c7134a8
                Copyright © © 2017 by the author.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 17 April 2017
                Date accepted : 12 July 2017
                Categories
                Subject: Review

                Keywords: ω-3 pufas,epa,dha,iga nephropathy,aspirin
                Data availability:
                Keywords: ω-3 pufas, epa, dha, iga nephropathy, aspirin

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