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首页> 外文期刊>Journal of psychiatric research >Peripheral eotaxin-1 (CCL11) levels and mood disorder diagnosis in a population-based sample of young adults
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Peripheral eotaxin-1 (CCL11) levels and mood disorder diagnosis in a population-based sample of young adults

机译:以人群为基础的年轻人样本中外周血中eotaxin-1(CCL11)水平和情绪障碍的诊断

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C-C motif chemokine 11 (CCL11) - or eotaxin-1 - is a small cytokine originally associated with chemotaxis (Van Coillie, Van Damme, & Opdenakker, 1999). CCL11 has a potent chemo attractant effect on eosinophils (hence eotaxin), inducing their accumulation at allergic inflammation sites. Neurons and glia both exhibit chemokine receptors, which lead to the interest in the effect of these cytokines in the CNS; furthermore, activation of the CCR3 receptor by CCL11 inhibits neural stem cell proliferation in the hippocampus (Krathwohl and Kaiser, 2004). Indeed, circulating CCL11, when increased, has been very convincingly demonstrated in a series of elegant experiments to cause the characteristic deficits in synaptic plasticity, neurogenesis and cognition that are associated with aging (Villeda et al, 2011). Further recent work suggests that CCL11 can influence neurogenesis through an impact on brain cytokine networks (Mendelsohn and Larrick, 2011). This chemokine inhibits IL-4 activity, providing another route whereby CCL11 can have an indirect impact on the brain (Derecki et al., 2010). This is relevant because it provides a level of explanation that ties central nervous system pathophysiology to the systemic milieu (Kapczinski et al., 2010; Villeda and Wyss-Coray, 2013).
机译:C-C基序趋化因子11(CCL11)-或eotaxin-1-是一种最初与趋化性相关的小细胞因子(Van Coillie,Van Damme和Opdenakker,1999)。 CCL11对嗜酸性粒细胞(因此嗜酸性粒细胞趋化因子)具有有效的化学引诱作用,诱导其在变应性炎症部位积聚。神经元和神经胶质细胞均显示趋化因子受体,这引起了对这些细胞因子在中枢神经系统中的作用的兴趣。此外,CCL11激活CCR3受体抑制了海马神经干细胞的增殖(Krathwohl和Kaiser,2004)。确实,循环CCL11含量增加时,已经在一系列优雅的实验中非常有力地证明了这一点,从而引起与衰老相关的突触可塑性,神经发生和认知功能缺陷(Villeda等,2011)。最近的进一步研究表明,CCL11可以通过影响脑细胞因子网络来影响神经发生(Mendelsohn和Larrick,2011)。这种趋化因子抑制IL-4活性,提供了另一种途径,使CCL11可以对大脑产生间接影响(Derecki等,2010)。这是相关的,因为它提供了将中枢神经系统病理生理与系统环境联系起来的某种解释水平(Kapczinski等人,2010; Villeda和Wyss-Coray,2013)。

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