de Almeida-Leite Camila Megale, Silva Isabel Cristina Costa, Galvão Lúcia Maria da Cunha, Arantes Rosa Maria Esteves
Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brasil.
Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brasil.
Mem Inst Oswaldo Cruz. 2014 Jul;109(4):459-65. doi: 10.1590/0074-0276130492.
Nitric oxide (NO) participates in neuronal lesions in the digestive form of Chagas disease and the proximity of parasitised glial cells and neurons in damaged myenteric ganglia is a frequent finding. Glial cells have crucial roles in many neuropathological situations and are potential sources of NO. Here, we investigate peripheral glial cell response to Trypanosoma cruzi infection to clarify the role of these cells in the neuronal lesion pathogenesis of Chagas disease. We used primary glial cell cultures from superior cervical ganglion to investigate cell activation and NO production after T. cruzi infection or lipopolysaccharide (LPS) exposure in comparison to peritoneal macrophages. T. cruzi infection was greater in glial cells, despite similar levels of NO production in both cell types. Glial cells responded similarly to T. cruzi and LPS, but were less responsive to LPS than macrophages were. Our observations contribute to the understanding of Chagas disease pathogenesis, as based on the high susceptibility of autonomic glial cells to T. cruzi infection with subsequent NO production. Moreover, our findings will facilitate future research into the immune responses and activation mechanisms of peripheral glial cells, which are important for understanding the paradoxical responses of this cell type in neuronal lesions and neuroprotection.
一氧化氮(NO)参与恰加斯病消化型的神经元损伤,受损肌间神经节中寄生的神经胶质细胞与神经元相邻是常见现象。神经胶质细胞在许多神经病理情况下发挥关键作用,并且是NO的潜在来源。在此,我们研究外周神经胶质细胞对克氏锥虫感染的反应,以阐明这些细胞在恰加斯病神经元损伤发病机制中的作用。我们使用来自颈上神经节的原代神经胶质细胞培养物,与腹腔巨噬细胞相比,研究克氏锥虫感染或脂多糖(LPS)暴露后细胞的激活和NO的产生。尽管两种细胞类型中NO产生水平相似,但克氏锥虫在神经胶质细胞中的感染更严重。神经胶质细胞对克氏锥虫和LPS的反应相似,但对LPS的反应比巨噬细胞弱。我们的观察结果有助于理解恰加斯病的发病机制,这基于自主神经胶质细胞对克氏锥虫感染高度敏感并随后产生NO。此外,我们的发现将促进未来对外周神经胶质细胞免疫反应和激活机制的研究,这对于理解这种细胞类型在神经元损伤和神经保护中的矛盾反应很重要。