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2
Rapid and sensitive diagnosis of fungal keratitis with direct PCR without template DNA extraction.直接 PCR 无需模板 DNA 提取即可快速灵敏地诊断真菌性角膜炎。
Clin Microbiol Infect. 2014 Oct;20(10):O776-82. doi: 10.1111/1469-0691.12571. Epub 2014 Mar 5.
3
Clinical observation of removal of the necrotic corneal tissue combined with conjunctival flap covering surgery under the guidance of the AS-OCT in treatment of fungal keratitis.AS-OCT引导下切除坏死角膜组织联合结膜瓣覆盖术治疗真菌性角膜炎的临床观察
Int J Ophthalmol. 2012;5(1):88-91. doi: 10.3980/j.issn.2222-3959.2012.01.18. Epub 2012 Feb 18.
4
[Signal transduction pathways mediated by Toll-like receptors and their relations with fungal keratitis].[Toll样受体介导的信号转导通路及其与真菌性角膜炎的关系]
Zhonghua Yan Ke Za Zhi. 2012 Jan;48(1):80-4.
5
Combined treatment with flap amputation, phototherapeutic keratectomy, and collagen crosslinking in severe intractable post-LASIK atypical mycobacterial infection with corneal melt.严重难治性 LASIK 后非典型分枝杆菌感染伴角膜融解采用瓣切除、光疗性角膜切削术和胶原交联联合治疗。
J Cataract Refract Surg. 2012 Apr;38(4):713-5. doi: 10.1016/j.jcrs.2012.01.009. Epub 2012 Feb 23.
6
Vitamin D enhances corneal epithelial barrier function.维生素 D 增强角膜上皮屏障功能。
Invest Ophthalmol Vis Sci. 2011 Sep 21;52(10):7359-64. doi: 10.1167/iovs.11-7605.
7
[Mechanism of the immune response to keratomycosis].
Zhonghua Yan Ke Za Zhi. 2011 Apr;47(4):378-81.
8
Distinct roles for Dectin-1 and TLR4 in the pathogenesis of Aspergillus fumigatus keratitis.Dectin-1 和 TLR4 在烟曲霉角膜炎发病机制中的不同作用。
PLoS Pathog. 2010 Jul 1;6(7):e1000976. doi: 10.1371/journal.ppat.1000976.
9
Cross-talk between vitamin D receptor (VDR)- and peroxisome proliferator-activated receptor (PPAR)-signaling in melanoma cells.黑色素瘤细胞中维生素D受体（VDR）信号与过氧化物酶体增殖物激活受体（PPAR）信号之间的相互作用。
Anticancer Res. 2009 Sep;29(9):3647-58.
10
Fungal keratitis: changing pathogens and risk factors.真菌性角膜炎：不断变化的病原体和危险因素
Cornea. 2009 Jul;28(6):638-43. doi: 10.1097/ICO.0b013e318191695b.

茄病镰刀菌感染期间人角膜上皮细胞中维生素D受体和杀菌肽的表达

Expression of vitamin D receptor and cathelicidin in human corneal epithelium cells during fusarium solani infection.

作者信息

Cong Lin, Xia Yi-Ping, Zhao Gui-Qiu, Lin Jing, Xu Qiang, Hu Li-Ting, Qu Jian-Qiu, Peng Xu-Dong

机构信息

Department of Ophthalmology, the Affiliated Hospital of Qingdao University, Qingdao 266000, Shandong Province, China.

出版信息

Int J Ophthalmol. 2015 Oct 18;8(5):866-71. doi: 10.3980/j.issn.2222-3959.2015.05.03. eCollection 2015.

DOI:10.3980/j.issn.2222-3959.2015.05.03
PMID:26558193
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4630991/
Abstract

AIM

To observe the expression of vitamin D receptor (VDR) in human specimen and immortalized human corneal epithelium cells (HCEC) when challenged with fusarium solani. Moreover, we decided to discover the pathway of VDR expression. Also, we would like to detect the expression of cathelicidin antimicrobial peptide (CAMP) in the downstream pathway of VDR.

METHODS

Immunohistochemistry was used to examine the VDR expression in HCEC from healthy and fungal keratitis patients. Real time quantitative polymerase chain reaction (qPCR) was performed to observe the messenger ribonucleic acid (mRNA) change of VDR when immortalized HCEC were challenged with fusarium solani for different hours. CAMP was detected at both mRNA and protein levels.

RESULTS

We found out that the VDR expression in fusarium solani keratitis patients' specimen was much more than that in healthy people. The mRNA and protein expression of VDR increased when we stimulated HCEC with fusarium solani antigen (P<0.01) and it could be inhibited by toll like receptor 2 (TLR2) monoclonal antibody. The CAMP expression was decreased because of fusarium solani antigen stimulation (P<0.01).

CONCLUSION

The VDR expression can be increased via TLR2/1-VDR pathway while the CAMP expression is decreased by the stimulation of fusarium solani antigen.

摘要

目的

观察人标本及永生化人角膜上皮细胞（HCEC）在茄病镰刀菌刺激下维生素D受体（VDR）的表达。此外，我们决定探寻VDR表达的途径。同时，我们希望检测VDR下游途径中cathelicidin抗菌肽（CAMP）的表达。

方法

采用免疫组织化学法检测健康人和真菌性角膜炎患者HCEC中VDR的表达。对永生化HCEC用茄病镰刀菌刺激不同时间后，采用实时定量聚合酶链反应（qPCR）观察VDR信使核糖核酸（mRNA）的变化。从mRNA和蛋白质水平检测CAMP。

结果

我们发现茄病镰刀菌角膜炎患者标本中VDR的表达远高于健康人。用茄病镰刀菌抗原刺激HCEC时，VDR的mRNA和蛋白质表达增加（P<0.01），且可被Toll样受体2（TLR2）单克隆抗体抑制。茄病镰刀菌抗原刺激导致CAMP表达降低（P<0.01）。

结论

VDR表达可通过TLR2/1-VDR途径增加，而茄病镰刀菌抗原刺激可使CAMP表达降低。