Mohsen Ebrahimi Monfared1, Shima Shapoori2, Ghasem Mosayebi2,3, Behzad Khansarinejad2,3, Ali Ghazavi2,4, Masoud Rezagholizamenjany5, Ali Ganji6,7. 1. Department of Neurology, School of Medicine, Arak University of Medical Sciences, Arak, Iran. 2. Department of Microbiology and Immunology, School of Medicine, Arak University of Medical Sciences, Arak, Iran. 3. Molecular and Medicine Research Center, Arak University of Medical Sciences, Arak, Iran. 4. Traditional and Complementary Medicine Research Center (TCMRC), Arak University of Medical Sciences, Arak, Iran. 5. School of Medicine, Arak University of Medical Sciences, Arak, Iran. 6. Department of Microbiology and Immunology, School of Medicine, Arak University of Medical Sciences, Arak, Iran, a.ganji@arakmu.ac.ir. 7. Molecular and Medicine Research Center, Arak University of Medical Sciences, Arak, Iran, a.ganji@arakmu.ac.ir.
Abstract
INTRODUCTION: Multiple sclerosis (MS) is a neuroinflammatory autoimmune disease which involves the central nervous -system. Although the primary cause of MS is obscure, effects of some cytokine and chemokine patterns in both innate and adaptive immune systems have been described. - Objectives: Since limited studies have examined the role of interleukin (IL)-11 and chemokine CCL27 in MS, we aimed to identify changes in IL-11 and CCL27 gene expression and serum levels in relapsing-remitting MS (RRMS) patients, treated with interferon (IFN)-β and glatiramer acetate (GA). METHODS: The serum level and gene expression of IL-11 and CCL27 were measured and compared between treatment-naïve MS patients and RRMS patients who were treated with high-dose IFN-β1a, low-dose IFN-β1a, IFN-β1b, and GA via enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction. RESULTS: A significant decrease was observed in the serum level of CCL27 in treatment-naïve patients and IFN-β1b-treated patients compared to the healthy controls. On the other hand, a significant increase was found in the protein level of CCL27 in low-dose and high-dose IFN-β1a groups compared to the treatment-naïve group. In addition, CCL27 gene expression was higher in patients treated with GA than in the treatment-naïve group. There were no significant changes in the gene expression or protein level of IL-11 in all experimental groups. Additionally, a positive correlation was found between IL-11 and CCL-27. CONCLUSION: Our results suggest the inflammatory role of CCL27 in MS patients, while IFN-β1a seems to play a compensatory role for this chemokine.
INTRODUCTION:Multiple sclerosis (MS) is a neuroinflammatory autoimmune disease which involves the central nervous -system. Although the primary cause of MS is obscure, effects of some cytokine and chemokine patterns in both innate and adaptive immune systems have been described. - Objectives: Since limited studies have examined the role of interleukin (IL)-11 and chemokine CCL27 in MS, we aimed to identify changes in IL-11 and CCL27 gene expression and serum levels in relapsing-remitting MS (RRMS) patients, treated with interferon (IFN)-β and glatiramer acetate (GA). METHODS: The serum level and gene expression of IL-11 and CCL27 were measured and compared between treatment-naïve MSpatients and RRMS patients who were treated with high-dose IFN-β1a, low-dose IFN-β1a, IFN-β1b, and GA via enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction. RESULTS: A significant decrease was observed in the serum level of CCL27 in treatment-naïve patients and IFN-β1b-treated patients compared to the healthy controls. On the other hand, a significant increase was found in the protein level of CCL27 in low-dose and high-dose IFN-β1a groups compared to the treatment-naïve group. In addition, CCL27 gene expression was higher in patients treated with GA than in the treatment-naïve group. There were no significant changes in the gene expression or protein level of IL-11 in all experimental groups. Additionally, a positive correlation was found between IL-11 and CCL-27. CONCLUSION: Our results suggest the inflammatory role of CCL27 in MSpatients, while IFN-β1a seems to play a compensatory role for this chemokine.