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      Targeting Cytokines for Morphine Tolerance: A Narrative Review

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          Abstract

          Background:

          Despite its various side effects, morphine has been widely used in clinics for decades due to its powerful analgesic effect. Morphine tolerance is one of the major side effects, hindering its long-term usage for pain therapy. Currently, the thorough cellular and molecular mechanisms underlying morphine tolerance remain largely uncertain.

          Methods

          We searched the PubMed database with Medical subject headings (MeSH) including ‘morphine tolerance’, ‘cytokines’, ‘interleukin 1’, ‘interleukin 1 beta’, ‘interleukin 6’, ‘tumor necrosis factor alpha’, ‘interleukin 10’, ‘chemokines’. Manual searching was carried out by reviewing the reference lists of relevant studies obtained from the primary search. The searches covered the period from inception to November 1, 2017.

          Results

          The expression levels of certain chemokines and pro-inflammatory cytokines were significantly increased in animal models of morphine tolerance. Cytokines and cytokine receptor antagonist showed potent effect of alleviating the development of morphine tolerance.

          Conclusion

          Cytokines play a fundamental role in the development of morphine tolerance. Therapeutics targeting cytokines may become alternative strategies for the management of morphine tolerance.

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          Most cited references101

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          Cytokine pathways and joint inflammation in rheumatoid arthritis.

          E. Choy, G Panayi (2001)
          Article 0 comments Cited 440 times – based on 0 reviews     Review now
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            IL-10 inhibits cytokine production by activated macrophages.

            D Fiorentino, A Zlotnik, T R Mosmann … (1991)
            IL-10 inhibits the ability of macrophage but not B cell APC to stimulate cytokine synthesis by Th1 T cell clones. In this study we have examined the direct effects of IL-10 on both macrophage cell lines and normal peritoneal macrophages. LPS (or LPS and IFN-gamma)-induced production of IL-1, IL-6, and TNF-alpha proteins was significantly inhibited by IL-10 in two macrophage cell lines. Furthermore, IL-10 appears to be a more potent inhibitor of monokine synthesis than IL-4 when added at similar concentrations. LPS or LPS- and IFN-gamma-induced expression of IL-1 alpha, IL-6, or TNF-alpha mRNA was also inhibited by IL-10 as shown by semiquantitative polymerase chain reaction or Northern blot analysis. Inhibition of LPS-induced IL-6 secretion by IL-10 was less marked in FACS-purified peritoneal macrophages than in the macrophage cell lines. However, IL-6 production by peritoneal macrophages was enhanced by addition of anti-IL-10 antibodies, implying the presence in these cultures of endogenous IL-10, which results in an intrinsic reduction of monokine synthesis after LPS activation. Consistent with this proposal, LPS-stimulated peritoneal macrophages were shown to directly produce IL-10 detectable by ELISA. Furthermore, IFN-gamma was found to enhance IL-6 production by LPS-stimulated peritoneal macrophages, and this could be explained by its suppression of IL-10 production by this same population of cells. In addition to its effects on monokine synthesis, IL-10 also induces a significant change in morphology in IFN-gamma-stimulated peritoneal macrophages. The potent action of IL-10 on the macrophage, particularly at the level of monokine production, supports an important role for this cytokine not only in the regulation of T cell responses but also in acute inflammatory responses.
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              Interleukin-10: new perspectives on an old cytokine.

              David Mosser, Xia Zhang (2008)
              Interleukin-10 (IL-10) has long been recognized to have potent and broad-spectrum anti-inflammatory activity, which has been unequivocally established in various models of infection, inflammation, and even in cancer. However, because of the marginal successes of the initial clinical trials using recombinant IL-10, some of the interest in this cytokine as an anti-inflammatory therapeutic has diminished. New work showing IL-10 production from regulatory T cells and even T-helper 1 T cells has reinvigorated the field and revealed the power of this cytokine to influence immune responses. Furthermore, new preclinical studies suggest that combination therapies, using antibodies to IL-10 along with chemotherapy, can be effective in treating bacterial, viral, or neoplastic diseases. Studies to understand IL-10 gene expression in the various cell types may lead to new therapeutics to enhance or inhibit IL-10 production. In this review, we summarize what is known about the regulation of IL-10 gene expression by various immune cells. We speculate on the promise that this cytokine holds to influence immune responses and mitigate immune pathologies.
              Article 0 comments Cited 303 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Curr Neuropharmacol
                Journal ID (iso-abbrev): Curr Neuropharmacol
                Journal ID (publisher-id): CN
                Title: Current Neuropharmacology
                Publisher: Bentham Science Publishers
                ISSN (Print): 1570-159X
                ISSN (Electronic): 1875-6190
                Publication date (Electronic): April 2019
                Publication date (Print): April 2019
                Volume: 17
                Issue: 4
                Pages: 366-376
                Affiliations
                Anesthesiology Institute, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan, , China; Department of Anesthesiology and Pain Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan, , China
                Author notes
                [* ]Address correspondence to this author at the Tongji Hospital, Tongji Medical college, Huazhong University of Science and Technology, Wuhan, China; Tel: +86 27 83662853; E-mail: 13971587381@ 123456163.com
                Article
                Publisher ID: CN-17-366
                DOI: 10.2174/1570159X15666171128144441
                PMC ID: 6482476
                PubMed ID: 29189168
                SO-VID: 16b44141-e086-45f4-a8b6-c6fd7448f057
                Copyright © © 2019 Bentham Science Publishers
                License:

                This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) ( https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                Date received : 09 August 2017
                Date revision received : 06 November 2017
                Date accepted : 23 November 2017
                Categories
                Subject: Article

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: morphine tolerance,pro-inflammatory cytokines,chemokines,anti-inflammatory cytokines,pain,glial cells
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: morphine tolerance, pro-inflammatory cytokines, chemokines, anti-inflammatory cytokines, pain, glial cells

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