Abstract
Purpose:
To observe the expression of vitamin D receptor (VDR) in human corneal epithelial cells. Meanwhile, we wanted to discover the role of 1,25(OH)2D3 when challenged with Aspergillus fumigatus (AF).
Methods:
Immunohistochemistry was taken to examine the VDR in corneal epithelium. PCR was performed to observe the mRNA change of VDR when immortalized human corneal epithelial cells (HCEC) were challenged with AF antigen. When treated with 1,25(OH)2D3, the TLR2, TLR4, Dectin-1 and cathelicidin antimicrobial peptide (CAMP) expression were detected by PCR and western blot. The expression of pro-inflammatory cytokines were detected at both mRNA and protein levels.
Results:
VDR was expressed in human corneal epithelium. The VDR mRNA expression increased when stimulated with AF antigen, and the TLR2 monoclonal antibody could inhibit the expression specifically (P<0.01). When pretreated HCEC with 1,25(OH)2D3 before AF stimulation, the TLR2, TLR4 and Dectin-1 expression were decreased apparently (P<0.01) while the expression of CAMP was risen (P<0.01). The expression of pro-inflammatory cytokines were down-regulated by 1,25(OH)2D3.
Conclusions:
VDR exists in human corneal epithelium and the expression can be increased via TLR2/1-VDR pathway when stimulated with AF antigen. 1,25(OH)2D3 can inhibit the expression of TLR2, TLR4 and Dectin-1 while increasing CAMP production. The effects can reduce the damage caused by pro-inflammatory cytokines and enhance the antibacterial effects by CAMP.