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      The effects of vasoactive intestinal peptide in the rat model of experimental autoimmune neuritis and the implications for treatment of acute inflammatory demyelinating polyradiculoneuropathy or Guillain–Barré syndrome

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          Abstract

          Background

          Guillain–Barré syndrome is an acute inflammatory demyelinating polyneuropathy that is characterized histologically by demyelination of peripheral nerves and nerve roots, infiltrates of T lymphocytes, and an inflammatory response that includes macrophage infiltrates. The aim of this study was to evaluate the effects of vasoactive intestinal peptide (VIP) in a rat model of experimental autoimmune neuritis (EAN).

          Methods

          Forty male Lewis rats were divided into a control group (N=10), an EAN group (N=10), an EAN group treated with 15 nmol of VIP (N=10), and an EAN group treated with 30 nmol of VIP (N=10). The rat model was created by subcutaneous injection of P2 polypeptide (200 µg P257–81) into the base of the tail. Intraperitoneal injection of VIP was given on day 7. Rats were weighed and functionally evaluated using an EAN score (0–10). On day 16, the rats were euthanized. The sciatic nerve was examined histologically and using immunohistochemistry with antibodies against CD8, CD68, and forkhead box p3 (Foxp3). Serum concentrations of IL-17 and interferon-α (IFN-α) were measured by ELISA on day 16 after creating the EAN model.

          Results

          The VIP-treated EAN groups had increased body weight and improved EAN scores compared with the untreated EAN group. CD8-positive and CD68-positive cells were significantly reduced in the EAN group treated with 30 nmol of VIP compared with 15 nmol of VIP. Foxp3-positive cells were significantly decreased in both EAN groups treated with VIP, and serum concentrations of IL-17 and IFN-α were significantly lower compared with the untreated EAN group ( P<0.05).

          Conclusion

          In a rat model of EAN, treatment with VIP resulted in functional improvement, reduced nerve inflammation, and decreased serum levels of inflammatory cytokines.

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          Most cited references 1

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          Guillain-Barré syndrome: epidemiology, pathophysiology and management.

          Guillain-Barré syndrome (GBS) is clinically defined as an acute peripheral neuropathy causing limb weakness that progresses over a time period of days or, at the most, up to 4 weeks. GBS occurs throughout the world with a median annual incidence of 1.3 cases per population of 100 000, with men being more frequently affected than women. GBS is considered to be an autoimmune disease triggered by a preceding bacterial or viral infection. Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus and Mycoplasma pneumoniae are commonly identified antecedent pathogens. In the acute motor axonal neuropathy (AMAN) form of GBS, the infecting organisms probably share homologous epitopes to a component of the peripheral nerves (molecular mimicry) and, therefore, the immune responses cross-react with the nerves causing axonal degeneration; the target molecules in AMAN are likely to be gangliosides GM1, GM1b, GD1a and GalNAc-GD1a expressed on the motor axolemma. In the acute inflammatory demyelinating polyneuropathy (AIDP) form, immune system reactions against target epitopes in Schwann cells or myelin result in demyelination; however, the exact target molecules in the case of AIDP have not yet been identified. AIDP is by far the most common form of GBS in Europe and North America, whereas AMAN occurs more frequently in east Asia (China and Japan). The prognosis of GBS is generally favourable, but it is a serious disease with a mortality of approximately 10% and approximately 20% of patients are left with severe disability. Treatment of GBS is subdivided into: (i) the management of severely paralysed patients with intensive care and ventilatory support; and (ii) specific immunomodulating treatments that shorten the progressive course of GBS, presumably by limiting nerve damage. High-dose intravenous immunoglobulin (IVIg) therapy and plasma exchange aid more rapid resolution of the disease. The predominant mechanisms by which IVIg therapy exerts its action appear to be a combined effect of complement inactivation, neutralisation of idiotypic antibodies, cytokine inhibition and saturation of Fc receptors on macrophages. Corticosteroids alone do not alter the outcome of GBS.
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            Author and article information

            Journal
            Drug Des Devel Ther
            Drug Des Devel Ther
            Drug Design, Development and Therapy
            Drug Design, Development and Therapy
            Dove Medical Press
            1177-8881
            2018
            06 November 2018
            : 12
            : 3817-3824
            Affiliations
            [1 ]Department of Neurology, The 2nd Affiliated Hospital of Harbin Medical University, Heilongjiang Province, Harbin 150001, People’s Republic of China
            [2 ]Department of Immunology, Harbin Medical University, Heilongjiang Province, Harbin 150081, People’s Republic of China, helenjh@ 123456126.com
            [3 ]Immunity & Infection Key Laboratory of Heilongjiang Province, Harbin Medical University, Heilongjiang Province, Harbin 150081, People’s Republic of China, helenjh@ 123456126.com
            Author notes
            Correspondence: Huan Ren, Department of Immunology, Harbin Medical University, No 157 Baojian Road, Nangang District, Heilongjiang Province, Harbin 150081, People’s Republic of China, Email helenjh@ 123456126.com
            Article
            dddt-12-3817
            10.2147/DDDT.S175331
            6228051
            © 2018 Jiao and Ren. This work is published and licensed by Dove Medical Press Limited

            The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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            Original Research

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