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中国真菌学杂志 2010, Vol. 5  Issue (3): 133-136.

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实验性小鼠皮肤着色真菌病MCP-1和MIP-2研究

柴宝1, 熊瑛2   

  1. 1. 广东医学院附属深圳南山医院皮肤科, 深圳, 518052;
    2. 南方医科大学附属深圳市妇幼保健院皮肤科, 深圳, 518052
  • 收稿日期:2010-03-29 出版日期:2010-06-28 发布日期:2010-06-28
  • 作者简介:柴宝,女(汉族),博士,副主任医师.E-mail:drchaibao@gmail.com
  • 基金资助:
    广东省深圳市南山区科技计划项目(南卫2008034)

Experimental study on the gene expression of MCP-1 and MIP-2 in chromomycosis in mice

CHAI Bao1, XIONG Ying2   

  1. 1. Department of Dermatology, Shenzhen Nanshan Hospital, affiliated to Guangdong Medical College;
    2. Department of Dermatology, Maternal and Child Hospital of Shenzhen, affiliated to Southern Medical University Shenzhen, Shenzhen 518052, China
  • Received:2010-03-29 Online:2010-06-28 Published:2010-06-28

摘要: 目的 观察小鼠皮肤着色真菌病模型发病过程中趋化性细胞因子MCP-1、MIP-2表达的动态变化,探讨其在宿主防御机制中的可能作用。方法 ICR小鼠分为3组,A组为健康小鼠足垫皮下接种灭活卡氏支孢霉悬液(1×108cfu/mL,0.025mL);B组为健康小鼠足垫皮下接种卡氏支孢霉悬液(1×108cfu/mL,0.025mL);C组为免疫抑制小鼠足垫皮下接种卡氏支孢霉悬液(1×108cfu/mL,0.025mL)。接种后第7天、30天、60天时用荧光实时定量PCR法检测皮损组织MCP-1及MIP-2的mRNA表达水平、ELISA法检测皮损组织匀浆中MCP-1及MIP-2蛋白水平。结果 接种后卡氏支孢霉悬液的B组7d时MCP-1、MIP-2表达水平明显高于30d、60d,且7d时B组MCP-1、MIP-2表达水平明显高于A组和C组,但30d、60d时A、B、C组之间无显著性差异。结论 在卡氏支孢霉所致的着色真菌病模型的发病过程中可能有MCP-1、MIP-2这两种趋化性细胞因子的参与。

关键词: 着色真菌病, 单核细胞趋化蛋白, 中性粒细胞趋化因子

Abstract: Objective To detect the gene expression of chemokines in mice model of skin chromomycosis and explore their roles in protective mechanism of the host.Methods Active or inactive C.carrion suspension (1 × 108 cfu/mL,0.025mL) was inoculated subcutaneously in the feet pads of healthy or immunosuppressive mice,respectively.mRNAs of MCP-1 and MIP-2 in the leision were examined by a real-time fluorescent quantitative PCR (FQ-PCR),and protein levels of MCP-1 and MIP-2 in the lesion tissue were examined by ELISA on day 7,30 and 60 after inoculation.Results Expression of MCP-1 and MIP-2 in healthy mice inoculated with active C.carrion on day 7 was higher than that on other days or that in other groups on day 7.But there were no significant differences on day 30 or day 60.Conclusions Both MCP-1 and MIP-2 possiblely participated in the pathogenesis of chromomycosis model due to C.carrion.

Key words: chromomycosis, MCP-1, MIP-2

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