Background: Systemic Lupus Erythematosus (SLE) is a chronic autoimmune inflammatory disease with extensive clinical features. The role of Interleukin 10 (IL-10) is to promote autoantibody production and autoreactive B cell proliferation. Interleukin 17 (IL-17) associated with pathogenesis of SLE and positively correlated with disease activity. Intraperitoneal pristane can induce lupus in mice. Mesenchymal stem cells secretome work in paracrine effects asanti-inflammatory and immunomodulation agent by suppressing autoreactive T and B cell, which play an important role in pathogenesis of SLE. The aim of this study is to evaluate effect of mesenchymal stem cells secretome on the expression of IL-10 and IL-17 in murine lupus models induced by pristane. Methods: A randomized experimental study, post-test only control group design, samples using 21 female Mus Musculus mice strain Balb/C, divided into 3 groups: control group with intraperitoneal injection of 0.5 mL of 0.9% NaCl, treatment group with intraperitoneal injection of 0.5 mL pristane, therapy group with intraperitoneal injection of 0.5 mL pristane and 0.45 mL of secretome. Statistical analysis using ANOVA test. A p-value < 0.05 was considered statistically significant. Results: The results showed significant relationship between control and pristane groups both at the levels of IL-17 (control 6.9±1.95,pristane 9.9±2.27, pristane+secretome 6.1±1.95 p=0.016), and there are significant differences in the expression of IL-10 in the control group vs pristane group (-4,42±1,43 per 100 lymphocyte; p=0,006), pristane group vs pristane+secretome group (4,00±1,43 per 100 lymphocyte; p=0,012). Conclusion: Mesenchymal stem cells secretome decreased the expression of IL-10 and IL-17 levels in murine lupus models induced by pristane.
CITATION STYLE
Nurudhin, A., Kertia, N., & Adnan, Z. A. (2017). Effect of secretome mesenchymal stem cells on expression interleukin 10 and interleukin 17 in mice lupus model. Bangladesh Journal of Medical Science, 16(3), 418–422. https://doi.org/10.3329/bjms.v16i3.32862
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