Effects of 25-hydroxyvitamin D3 on cathelicidin production and antibacterial function of human oral keratinocytes

被引:16
作者
Wang, Qi [1 ,2 ]
Zhang, Wu [2 ]
Li, Hao [1 ]
Aprecio, Raydolf [2 ]
Wu, Wan [3 ]
Lin, Yiqiao [2 ]
Li, Yiming [2 ]
机构
[1] Sichuan Univ, West China Hosp Stomatol, State Key Lab Oral Dis, Chengdu 610041, Peoples R China
[2] Loma Linda Univ, Sch Dent, Dent Res Ctr, Loma Linda, CA 92354 USA
[3] Wenzhou Med Coll, Affiliated Hosp 1, Wenzhou 325000, Peoples R China
基金
中国国家自然科学基金;
关键词
25-Hydroxyvitamin D-3; Oral keratinocytes; Cathelicidin; 1 alpha-Hydroxylase (CYP27B1); 24-Hydroxylase (CYP24A1); VITAMIN-D; EPITHELIAL-CELLS; ANTIMICROBIAL PEPTIDES; MYCOBACTERIUM-TUBERCULOSIS; 1,25-DIHYDROXYVITAMIN D-3; INNATE IMMUNITY; PROSTATE CELLS; EXPRESSION; INDUCTION; ACTINOMYCETEMCOMITANS;
D O I
10.1016/j.cellimm.2013.06.007
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Vitamin D and its metabolites have been recognized as key determinants in innate immune modulation. In this study, we investigated the regulation of antibacterial functions of oral keratinocyte cells by 25-hydroxyvitamin D-3 (25VD(3)). OKF6/TERT2 cells, an immortalized human oral keratinocyte cell line, were transfected with or without 24-hydroxylase small interfering RNA (siRNA) and incubated with different amounts of 25VD(3). These epithelial cells expressed high levels of inactivating 24-hydroxylase (CYP24A1) and relatively low levels of activating 1 alpha-hydroxylase (CYP27B1) in the presence of 25VD(3). 25VD(3) influenced the expression of vitamin D-driven genes and cathelicidin in a dose-related manner. SiRNA specific to 24-hydroxylase augmented the cathelicidin production and subseqently influenced the antibacterial activity on multispecies of oral pathogens. These observations suggest that 25VD(3) is capable of stimulating cathelicidin production and modulating antibacterial function upon CYP24A1 knochdown in oral epithelial cells, and indicate novel mechanisms that 25VD(3) may enhance antibacterial ability in oral keratinocytes. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:45 / 50
页数:6
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