Capsaicin induces high expression of BAFF and aberrantly glycosylated IgA1 of tonsillar mononuclear cells in IgA nephropathy patients

被引:12
|
作者
Shao, Jing [1 ]
Peng, Youming [1 ]
He, Liyu [1 ]
Liu, Hong [1 ]
Chen, Xian [1 ]
Peng, Xiaofei [1 ]
机构
[1] Cent S Univ, Xiangya Hosp 2, Dept Nephrol, Hunan Key Lab Kidney Dis & Blood Purificat, Changsha 410011, Hunan, Peoples R China
基金
中国国家自然科学基金;
关键词
Capsaicin; BAFF; C1GALT1; Cosmc; IgA nephropathy; MASS-SPECTROMETRY; TONSILLECTOMY; BETA-1,3-GALACTOSYLTRANSFERASE; SUSCEPTIBILITY; INCREASE; THERAPY; CLONING;
D O I
10.1016/j.humimm.2014.08.205
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Background: IgA nephropathy (IgAN) is the most common type of primary glomerulonephritis in the world. Hot pepper is the most favorite vegetable for Chinese in Hunan and Sichuan provinces. It can be assumed that capsaicin, the active ingredient of hot pepper, is a possible risk factor in diet in the pathogenesis of IgAN. Methods: 22 subjects, including 11 IgAN patients and 11 non-IgAN patients were enrolled in this study. Tonsillar mononuclear cells were isolated and cultured for 3 days with or without capsaicin. Results: In the absence and presence of capsaicin, the BAFF expression and IgA1 secretion were higher in IgAN patients than that in non-IgAN patients, meanwhile, the gene expression of C1GALT1 and Cosmc and IgA1 O-glycosylation level were significantly lower. In IgAN group, coincubated with capsaicin, IgA1 and BAFF secretion and BAFF expression by TMCs were significantly higher than that without capsaicin, furthermore, the level of mRNA encoding C1GALT1 and Cosmc and the level of IgA1 O-glycosylation were evidently lower. Conclusion: Capsaicin may induce IgA1 secretion by activating BAFF expression, and bring to aberrantly IgA1 O-glycosylation by suppressing C1GALT1 and Cosmc expression. Therefore, to limit the consumption of hot pepper would be beneficial to patients with IgA nephropathy. (C) 2014 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:1034 / 1039
页数:6
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