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Serum CCL20 and Its Association with SIRT1 Activity in Multiple Sclerosis Patients

Li, R., Sun, X., Shu, Y., Wang, Y., Xiao, L., Wang, Z., Hu, X., Kermode, A.G. and Qui, W. (2018) Serum CCL20 and Its Association with SIRT1 Activity in Multiple Sclerosis Patients. Multiple Sclerosis Journal, 24 (3). p. 390.

Link to Published Version: https://doi.org/10.1177/1352458517751792
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Abstract

Background: CCL20, an inflammatory chemokine, is a potentially important component in the pathogenesis of MS. SIRT1 exhibits a negative regulatory effect on a variety of inflammatory cytokines and can relieve EAE. The association between the level of CCL20 and SIRT1 expression in MS patients has not been investigated.

Methods: Blood samples were collected from 38 RRMS patients and 40 healthy controls. Serum and peripheral blood mononuclear cells (PBMCs) were purified. The serum levels of CCL20 were measured by ELISA. Sirt1 activity was evaluated from total protein of PBMC samples by fluorometric assay. PBMC total histone was extracted, and PBMC Global histone H3/H4 acetylation and H3K9 acetylation status were assessed by EpiQuik™ global histoneH3/H4 acetylation and H3K9 acetylation quantification Kit.

Results: Serum levels of CCL20 were significantly higher in MS patients compared with controls. A statistically significant decrease in SIRT1 activity was seen in MS patients with relapse compared to controls. Pearson’s correlation test showed that serum CCL20 levels were negatively correlated with SIRT1 concentrations (R = −0.331, p = 0.042). SIRT1 activity was negatively correlated with H3K9 acetylation (R = −0.335, p = 0.040).

Conclusion: Elevated serum CCL20 concentrations were observed in MS, and there was an association between CCL20 and SIRT1 activity in MS patients.

Item Type: Journal Article
Murdoch Affiliation(s): Institute for Immunology and Infectious Diseases
Publisher: Sage Publications
Copyright: © 2018 by SAGE Publications
Other Information: Poster presentation for PACTRIMs 2017
URI: http://researchrepository.murdoch.edu.au/id/eprint/40812
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