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鼠眼弓形虫病中细胞因子、趋化因子、趋化因子受体和黏附分子的动力学分析。

Kinetic analysis of cytokines, chemokines, chemokine receptors and adhesion molecules in murine ocular toxoplasmosis.

机构信息

Department of Infection and Host Defense, Graduate School of Medicine, Chiba University, Chiba, Japan.

出版信息

Br J Ophthalmol. 2012 Sep;96(9):1259-67. doi: 10.1136/bjophthalmol-2012-301490. Epub 2012 Jul 11.

Abstract

BACKGROUND/AIMS: To investigate the molecules possibly influencing the recruitment and migration of leucocytes in murine ocular toxoplasmosis, the kinetics of the messenger RNA expression levels of cytokines, chemokines, chemokine receptors and adhesion molecules in the retina were analysed.

METHODS

Retina and brain were obtained sequentially from Toxoplasma gondii Fukaya strain-infected wild-type (WT) C57BL/6 and interferon gamma (IFN-γ) knockout (GKO) mice of the same background. The mRNA expression levels of these molecules were analysed by real-time PCR assay.

RESULTS

In the retina of WT mice the expression levels of IFN-γ, interleukin 17A, CCL3, CCL4, CCL5, CXCL1, CXCL2, CXCL10, CCR5, CCR7, CXCR2, CXCR3 and intracellular adhesion molecule 1 increased, reaching peaks approximately 14-28 days after infection. The expression levels of CXCR4 and CXCR5 were absent and very low, respectively, during the infection. In the brain of WT mice, the kinetic patterns of these expression levels tended to be the same as in the retina except CXCR4. On the other hand, in GKO mice these molecules, except CXCL1, CXCL2 and CXCR2, remained at basal levels.

CONCLUSION

In murine ocular toxoplasmosis, cytokines, chemokines, chemokine receptors and adhesion molecules were involved in the pathogenesis, and IFN-γ played a pivotal role.

摘要

背景/目的:为了研究可能影响鼠眼弓形虫病中白细胞募集和迁移的分子,分析了细胞因子、趋化因子、趋化因子受体和黏附分子信使 RNA 表达水平在视网膜中的动力学变化。

方法

从同一背景的弓形虫福冈株感染的野生型(WT)C57BL/6 和干扰素γ(IFN-γ)敲除(GKO)小鼠中依次获得视网膜和脑组织。通过实时 PCR 检测分析这些分子的 mRNA 表达水平。

结果

在 WT 小鼠的视网膜中,IFN-γ、白细胞介素 17A、CCL3、CCL4、CCL5、CXCL1、CXCL2、CXCL10、CCR5、CCR7、CXCR2、CXCR3 和细胞间黏附分子 1 的表达水平增加,在感染后约 14-28 天达到峰值。在感染过程中,CXCR4 的表达水平很低,几乎不存在。在 WT 小鼠的大脑中,这些表达水平的动力学模式与视网膜相似,但 CXCR4 除外。另一方面,在 GKO 小鼠中,除 CXCL1、CXCL2 和 CXCR2 外,这些分子的表达水平保持在基础水平。

结论

在鼠眼弓形虫病中,细胞因子、趋化因子、趋化因子受体和黏附分子参与了发病机制,IFN-γ 发挥了关键作用。

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