Neuroimmunomodulation · 2020
Assessment of CCL27 and IL-11 in Multiple Sclerosis Patients Treated with Interferon-β and Glatiramer Acetate.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Ebrahimi Monfared Mohsen, Shapoori Shima, Mosayebi Ghasem, Khansarinejad Behzad, Ghazavi Ali, Rezagholizamenjany Masoud, Ganji Ali
Аннотация
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.
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.