Eosinophil chemotactic chemokine profilings of the brain from permissive and non-permissive hosts infected with Angiostrongylus cantonenis
Eosinophil chemotactic chemokine profilings of the brain from permissive and non-permissive hosts infected with Angiostrongylus cantonenis
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感染广州管圆线虫的允许和非允许宿主大脑的嗜酸性粒细胞趋化因子分析
DOI：
10.1007/s00436-013-3683-x
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发表时间：
2014-02-01
影响因子：
2
通讯作者：
Lv, Zhiyue
中科院分区：
文献类型：
--
作者：
Li, Shuting;Yang, Fan;Lv, Zhiyue
广州管圆线虫的入侵主要引起严重或轻微的嗜酸性粒细胞脑膜炎和脑膜脑炎，分别在非许可和许可的主机。趋化因子是一种有效的白细胞趋化因子，可能在介导嗜酸性粒细胞募集中发挥重要作用。在本研究中，我们比较分析了外周血和脑脊液嗜酸性粒细胞计数的变化，以及嗜酸性粒细胞趋化因子的表达谱。广州杆菌感染小鼠（CCL 2、CCL 3、CCL 5、CCL 7、CCL 8、CCL 11、CCL 12、CCL 24和CCL 28）和大鼠在感染后1、2、5、7、14和21天（dpi）探索CCL 2、CCL 3、CCL 5、CCL 11和CCL 12，感染后5 d，感染小鼠的血液和脑脊液中嗜酸性粒细胞数量显著增加，而感染大鼠的血液和脑脊液中嗜酸性粒细胞数量分别在感染后5 d和14 d显著增加。CSF嗜酸性粒细胞增多的动力学基本上与各时间点感染动物脑中嗜酸性粒细胞趋化因子水平相关。有趣的是，与小鼠相比，在大鼠中观察到更少的CSF嗜酸性粒细胞和脑中嗜酸性粒细胞浸润，尽管在21 dpi时感染大鼠的脑中也维持极高水平的趋化因子。我们进一步描述了CCL 11（嗜酸细胞趋化因子），一种先前报道的嗜酸细胞趋化因子在管圆线虫病中，主要从感染A的小鼠和大鼠的活化小胶质细胞释放。广东话。我们的研究结果表明，不同的复杂的趋化因子网络介导的招募嗜酸性粒细胞之间的许可和非许可的主机在A。为临床治疗广州管圆线虫病提供了有希望的靶点。
Angiostrongylus cantonensisinvasion primarily cause heavy or negligible eosinophic meningitis and meningoencephalitis in the brain of non-permissive and permissive hosts, respectively. Chemokines are effective leukocyte chemoattractants and may play an essential role in mediating eosinophil recruitment in angiostrongyliasis. In the present study, we comparatively analyzed changes in peripheral and CSF eosinophil counts, and expression profilings of eosinophil chemotactic chemokines inA. cantonensis-infected mice (CCL 2, CCL 3, CCL 5, CCL7, CCL 8, CCL 11, CCL 12, CCL 24 and CCL 28) and rats (CCL 2, CCL 3, CCL 5, CCL 11 and CCL 12) were explored at 1, 2, 5, 7, 14, and 21 days post-infection (dpi), and found significantly elevated numbers of eosinophils in blood and CSF of infected mice after 5 dpi, while significant increases of eosinophils in blood and CSF of infected rats were detected after 5 and 14 dpi, respectively. The kinetics of CSF eosinophilia is basically correlated with eosinophil chemotactic chemokine levels in brains of infected animals at each time point. Interestingly, less CSF eosinophils and infiltration of eosinophils in the brain were noted in rats than in mice, though extremely high levels of chemokines were also maintained in the brains of infected rats at 21 dpi. We further described CCL 11 (eotaxin), a previously reported eosinophil chemotactic factor in angiostrongyliasis, was mainly released from activated microglia in mice and rats infected withA. cantonensis. Our results reveal that different complicated chemokine networks mediate recruitment of eosinophils between permissive and non-permissive hosts duringA. cantonensisinfection, and provide promising targets for clinical treatment of angiostrongyliasis.