DC-SIGN基因在阿萨希毛孢子菌小鼠皮肤感染时的表达与调控  

Expression and regulation of DC-SIGN gene in cutaneous Trichosporon asahii infection in mice

作　　者：王文岭[1] 杨蓉娅[1] 郝震锋[1] 敖俊红[1] 赵逊[1] 张洁[1] 王聪敏[1] 

机构地区：[1]北京军区总医院全军皮肤病诊疗中心,北京100700

出　　处：《解放军医学杂志》2008年第4期462-464,共3页Medical Journal of Chinese People's Liberation Army

基　　金：中华医学会皮肤科分会(诺华)基金资助课题(DEM075);国家自然科学基金资助课题(30570099)

摘　　要：目的了解树突细胞C型凝集素(DC-SIGN)是否参与了皮肤毛孢子菌感染过程中的免疫应答。方法25只BALB/C小鼠备皮后皮下接种3.2×107cfu/ml的阿萨希毛孢子菌悬液,分别于接种后1、3、7、14d处死小鼠,切取皮损,RT-PCR检测皮肤毛孢子菌感染过程中DC-SIGN mRNA的表达,基因芯片技术观察免疫相关基因的改变。结果皮下接种后3、7、14d接种侧皮肤组织标本可扩增出DC-SIGN目的片段,而未接种侧皮肤组织标本均未扩增出DC-SIGN目的片段。补体C2、前列腺素EP4受体、肿瘤坏死因子诱导蛋白cg12-1(CG12-1)、干扰素诱导蛋白(Ifit3)、淋巴细胞抗原6复合物、CD53抗原、CD22抗原等下调。结论DC-SIGN参与了皮肤毛孢子菌的感染过程,它不仅抑制Th1型细胞免疫,而且可抑制前列腺素EP4受体及部分补体因子等,从而导致皮肤毛孢子菌感染的慢性化。Objective Dentritic cell-specific ICAM-3 grabbing nonintegrin （DC-SIGN） is an important receptor for pathogenic microbes, and it acts as pathogen-recognition receptor （PAMP） and provides a bridge between the innate immunity and acquired immunity. It is meaningful to clarify whether DC-SIGN takes part in the course of cutaneous Trichosporon asahii infection and how it manages the other cytokines. Methods Twenty-five male mice were hypodermically injected with 3.2×107 CFU/ml of Trichosporon asahii suspension on one side of the back, the other side of the back received no injection to serve as control. Another five mice were treated with 0.9% saline solution as control. The cutaneous specimens were obtained on the 1st, 3rd, 7th and 14th day after inoculation. The expression of DC-SIGN gene and the other genes related to cutaneous immunity after cutaneous infection of Trichosporon asahii were investigated by RT-PCR and microarray. Results The DC-SIGN products containing 242 bp of nucleic acid from the skin specimens of the inoculated sites were amplified with RT-PCR on the 3rd, 7th and 14th day after inoculation. The results of microarray showed that a series of genes were down-regulated, including complement component 2, TNF-inducible protein cg12-1 （CG12-1）, interferon-induced protein with tetratricopeptide repeats 3 （Ifit3）, CD53 antigen, CD22 antigen, and prostaglandin E receptor 4. Conclusions The results suggest that DC-SIGN takes part in the course of Trichosporon asahii infection. DC-SIGN not only inhibits Th1 type of cell-mediated immunity, but also inhibits some of complement factors, prostaglandin E receptor and immunoglobulin binding protein 1b, thus resulting in chronic and intractable infection of Trichosporon asahii. The detailed roles of DC-SIGN in the course need to be further studied.

关 键 词：毛孢子菌属 树突细胞C型凝集素 反转录聚合酶链反应 

分 类 号：R446.53[医药卫生—诊断学]