Foxp3-positive cells were significantly decreased in both EAN groups treated with VIP, and serum concentrations of IL-17 and IFN- were significantly lower compared with the untreated EAN group ( em P /em 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. strong class=”kwd-title” Keywords: Guillain, Barr syndrome, vasoactive intestinal peptide, experimental autoimmune neuritis, acute inflammatory demyelinating polyradiculoneuropathy Introduction Worldwide, GuillainCBarr syndrome (GBS), also known as acute inflammatory demyelinating polyradiculoneuropathy, is a neurological condition that can occur in otherwise healthy adults and at any age, with a reported incidence of 1C4 per 100,000 individuals.1,2 VTP-27999 Owing to the improvements in the diagnosis of GBS, the disease has been shown to have an increasing incidence rate.3,4 Also, although immunoglobulin and plasma therapy have shortened the recovery time for the GBS, patients with GBS still have a mortality rate of 2%C8%, and ~20% of patients with GBS will not recover completely, but will have long-term neurological sequelae.5 Therefore, further studies VTP-27999 on the pathogenesis of GBS and effective treatment methods continue to be important. GBS 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 rat model was created by subcutaneous injection of P2 polypeptide (200 g P257C81) 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 (0C10). On day 16, the rats were euthanized. The sciatic VTP-27999 nerve was examined histologically and using immunohistochemistry with antibodies against CD8, CD68, and forkhead box p3 (Foxp3). Serum concentrations of IL-17 and interferon- (IFN-) 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- were significantly lower Keratin 7 antibody compared with the untreated EAN group ( em P /em 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. strong class=”kwd-title” Keywords: Guillain, Barr syndrome, vasoactive intestinal peptide, experimental autoimmune neuritis, acute inflammatory demyelinating polyradiculoneuropathy Introduction Worldwide, GuillainCBarr syndrome (GBS), also known as acute inflammatory demyelinating polyradiculoneuropathy, is a neurological condition that can occur in otherwise healthy adults and at any age, with a reported incidence of 1C4 per 100,000 individuals.1,2 Owing to the improvements in the diagnosis of GBS, the disease has been shown to have an increasing incidence rate.3,4 Also, although immunoglobulin and plasma therapy have VTP-27999 shortened the recovery time for the GBS, patients with GBS still have a mortality rate of 2%C8%, and ~20% of patients with GBS will not recover completely, but will have long-term neurological sequelae.5 Therefore, further studies on the pathogenesis of GBS and effective treatment methods continue to be important. GBS 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 etiology of GBS is currently unclear, but it is known to be associated with a CD4 T-cell-mediated autoimmune response.6,7 The cytokines secreted by CD4 cells play an important role in initiating and regulating tissue-specific autoimmune responses and include pro-inflammatory cytokines and anti-inflammatory cytokines, with the balance between the two having an important effect on the progression of GBS. Experimental autoimmune neuritis (EAN) is an established animal model of acute inflammatory demyelinating polyradiculoneuropathy, or GBS. Rodent models of EAN can be established using injections of P2 protein into nerve roots. Vasoactive intestinal peptide (VIP) has important regulatory roles in the physiological and immune systems of the body, including T-cell and B-cell immune responses. Previously published studies have shown that B cells and the production of antibodies also have a VTP-27999 role in the pathogenesis of both EAN and GBS.8 The aim of the present study was to evaluate the effects of two dose regimes of VIP in an established rat model of EAN and to evaluate the effects of treatment on neurological function, nerve inflammation, and serum levels of inflammatory cytokines, IL-17 and interferon- (IFN-). Materials and methods Ethical approval The procedures for care and use of animals were approved by the Ethics Committee of the second Affiliated Hospital of Harbin Medical University and all applicable institutional and governmental regulations concerning the ethical use of animals were followed. Preparation of the P257C81 polypeptide antigen emulsion Tuberculin was weighed and mixed with incomplete Freunds adjuvant in a tube for the preparation of complete.