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      Fundamentals of and Critical Issues in Lipid Autacoid Medicine: A Review

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          Abstract

          The identification of a number of families of lipid signal molecules since the 1990s created new therapeutic possibilities for a great number of disorders characterized by chronic inflammation and pain. These lipid autacoids have been explored in a great variety of animal models related to inflammation, pain, (neuro-)protection, and repair. Based on the data from these models, as well as on a number of proof of principle studies in the clinic in indications such as neuropathic pain, a new chapter in medicine is about to begin. We would like to introduce the term “Autacoid Pain Medicine” for this chapter. There are, however, a number of methodological and strategic issues to overcome in this field. One of the roadblocks is related to patent strategies around families of these molecules. As this is not always recognized we will present a number of examples.

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          Resolvins RvE1 and RvD1 attenuate inflammatory pain via central and peripheral actions.

          Tong-Zu Liu, J. Park, Temugin Berta … (2010)
          Inflammatory pain, such as arthritis pain, is a growing health problem. Inflammatory pain is generally treated with opioids and cyclooxygenase (COX) inhibitors, but both are limited by side effects. Recently, resolvins, a unique family of lipid mediators, including RvE1 and RvD1 derived from omega-3 polyunsaturated fatty acid, have shown marked potency in treating disease conditions associated with inflammation. Here we report that peripheral (intraplantar) or spinal (intrathecal) administration of RvE1 or RvD1 in mice potently reduces inflammatory pain behaviors induced by intraplantar injection of formalin, carrageenan or complete Freund's adjuvant (CFA), without affecting basal pain perception. Intrathecal RvE1 injection also inhibits spontaneous pain and heat and mechanical hypersensitivity evoked by intrathecal capsaicin and tumor necrosis factor-alpha (TNF-alpha). RvE1 has anti-inflammatory activity by reducing neutrophil infiltration, paw edema and proinflammatory cytokine expression. RvE1 also abolishes transient receptor potential vanilloid subtype-1 (TRPV1)- and TNF-alpha-induced excitatory postsynaptic current increases and TNF-alpha-evoked N-methyl-D-aspartic acid (NMDA) receptor hyperactivity in spinal dorsal horn neurons via inhibition of the extracellular signal-regulated kinase (ERK) signaling pathway. Thus, we show a previously unknown role for resolvins in normalizing the spinal synaptic plasticity that has been implicated in generating pain hypersensitivity. Given the potency of resolvins and the well-known side effects of opioids and COX inhibitors, resolvins may represent new analgesics for treating inflammatory pain.
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            Nerve growth factor: from neurotrophin to neurokine.

            Rita Levi-Montalcini, Stephen Skaper, Roberto Dal Toso … (1996)
            Nerve growth factor (NGF) is largely known as a target-derived factor responsible for the survival and maintenance of the phenotype of specific subsets of peripheral neurones and basal forebrain cholinergic nuclei during development and maturation. However, NGF also exerts a modulatory role on sensory, nociceptive nerve physiology during adulthood that appears to correlate with hyperalgesic phenomena occurring in tissue inflammation. Other NGF-responsive cells are now recognized as belonging to the haemopoietic-immune system and to populations in the brain involved in neuroendocrine functions. The concentration of NGF is elevated in a number of inflammatory and autoimmune states in conjunction with an increased accumulation of mast cells. Mast cells and NGF appear to be involved in neuroimmune interactions and tissue inflammation, with NGF acting as a general 'alert' molecule capable of recruiting and priming tissue defence processes following insult as well as systemic defensive mechanisms. Moreover, mast cells themselves produce NGF, suggesting that alterations in normal mast cell behaviours can provoke maladaptive neuroimmune tissue responses whose consequences could have profound implications in inflammatory disease states. This review discusses recent discoveries involving novel and diverse biological activities of this fascinating molecule.
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              Pro-Resolving Lipid Mediators Improve Neuronal Survival and Increase Aβ42 Phagocytosis.

              Mingqin Zhu, Xiuzhe Wang, Erik Hjorth … (2016)
              Inflammation in the brain is a prominent feature in Alzheimer's disease (AD). Recent studies suggest that chronic inflammation can be a consequence of failure to resolve the inflammation. Resolution of inflammation is mediated by a family of lipid mediators (LMs), and the levels of these specialized pro-resolving mediators (SPMs) are reduced in the hippocampus of those with AD. In the present study, we combined analysis of LMs in the entorhinal cortex (ENT) from AD patients with in vitro analysis of their direct effects on neurons and microglia. We probed ENT, an area affected early in AD pathogenesis, by liquid chromatography-tandem mass spectrometry (LC-MS-MS), and found that the levels of the SPMs maresin 1 (MaR1), protectin D1 (PD1), and resolvin (Rv) D5, were lower in ENT of AD patients as compared to age-matched controls, while levels of the pro-inflammatory prostaglandin D2 (PGD2) were higher in AD. In vitro studies showed that lipoxin A4 (LXA4), MaR1, resolvin D1 (RvD1), and protectin DX (PDX) exerted neuroprotective activity, and that MaR1 and RvD1 down-regulated β-amyloid (Aβ)42-induced inflammation in human microglia. MaR1 exerted a stimulatory effect on microglial uptake of Aβ42. Our findings give further evidence for a disturbance of the resolution pathway in AD, and indicate that stimulating this pathway is a promising treatment strategy for AD.
              Article 0 comments Cited 81 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Jan M. Keppel Hesselink:
                ORCID: http://orcid.org/0000-0002-0186-8050
                neuropathie7@gmail.com
                Journal
                Journal ID (nlm-ta): Pain Ther
                Journal ID (iso-abbrev): Pain Ther
                Title: Pain and Therapy
                Publisher: Springer Healthcare (Cheshire )
                ISSN (Print): 2193-8237
                ISSN (Electronic): 2193-651X
                Publication date (Electronic): 19 June 2017
                Publication date PMC-release: 19 June 2017
                Publication date (Print): December 2017
                Volume: 6
                Issue: 2
                Pages: 153-164
                Affiliations
                Institute for Neuropathic Pain, Bosch en Duin, Utrecht, The Netherlands
                Author information
                http://orcid.org/0000-0002-0186-8050
                Article
                Publisher ID: 75
                DOI: 10.1007/s40122-017-0075-4
                PMC ID: 5693806
                PubMed ID: 28631063
                SO-VID: 10921794-f7dd-4a4e-b85d-a328efe64fc1
                Copyright © © The Author(s) 2017
                History
                Date received : 8 May 2017
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © Springer Healthcare Ltd., part of Springer Nature 2017

                Keywords: aliamides,analgesia,autacoids,endocannabinoids,lipoxins,pain,palmitoylethanonolamide,phospholipids,protectins,resolvins,treatment
                Data availability:
                Keywords: aliamides, analgesia, autacoids, endocannabinoids, lipoxins, pain, palmitoylethanonolamide, phospholipids, protectins, resolvins, treatment

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