Portes Alex, Giestal-de-Araujo Elizabeth, Fagundes Aline, Pandolfo Pablo, de Sá Geraldo Arnaldo, Lira Marie Luce Flores, Amaral Veronica Figueiredo, Lagrota-Candido Jussara
Laboratório de Imunopatologia, Departamento de Imunobiologia, Universidade Federal Fluminense, Rio de Janeiro, Brazil.
Laboratório de Cultura de Tecidos Hertha Meyer, Departamento de Neurobiologia, Universidade Federal Fluminense, Rio de Janeiro, Brazil.
J Neuroimmunol. 2016 Dec 15;301:65-73. doi: 10.1016/j.jneuroim.2016.11.003. Epub 2016 Nov 12.
Neurological symptoms have been associated with Leishmania infection, however little is known about how the nervous system is affected in leishmaniasis. This work aimed to analyze parasitic load, production of cytokines/neurotrophins in the prefrontal cortex and behavioral changes in BALB/c mice infected with Leishmania amazonensis. At 2 and 4months post-infection, infected mice showed a decrease in IFN-γ, IL-1, IL-6, IL-4, IL-10 cytokines and BDNF and NGF neurotrophins in prefrontal cortex associated with increased anxiety behavior. Parasite DNA was found in brain of all animals at 4months post-infection, when the levels of IBA-1 (activated macrophage/microglia marker) and TNF-α was increased in the prefrontal cortex. However TNF-α returned to normal levels at 6months post-infection suggesting a neuroprotective mechanism.
神经症状与利什曼原虫感染有关,然而对于利什曼病中神经系统如何受到影响却知之甚少。这项研究旨在分析感染亚马逊利什曼原虫的BALB/c小鼠的寄生虫负荷、前额叶皮质中细胞因子/神经营养因子的产生以及行为变化。在感染后2个月和4个月时,感染小鼠前额叶皮质中的IFN-γ、IL-1、IL-6、IL-4、IL-10细胞因子以及BDNF和NGF神经营养因子减少,同时焦虑行为增加。在感染后4个月时,所有动物的大脑中均发现了寄生虫DNA,此时前额叶皮质中IBA-1(活化巨噬细胞/小胶质细胞标志物)和TNF-α的水平升高。然而,在感染后6个月时,TNF-α恢复到正常水平,提示存在一种神经保护机制。