Souza Viviane do Carmo Gonçalves, Dos Santos Joabel Tonellotto, Cabral Fernanda Licker, Barbisan Fernanda, Azevedo Maria Isabel, Dias Carli Luiz Felipe, de Avila Botton Sonia, Dos Santos Jaques Jeandre Augusto, Rosa Leal Daniela Bitencourt
Department of Microbiology and Parasitology, Health Sciences Center, Federal University of Santa Maria, Santa Maria, RS 97105-900, Brazil.
Department of Large Animal Clinic de Clínica, Rural Sciences Center, Federal University of Santa Maria, Santa Maria, RS 97105-900, Brazil.
Microb Pathog. 2017 Mar;104:32-38. doi: 10.1016/j.micpath.2017.01.002. Epub 2017 Jan 3.
Chagas disease (CD) is caused by Trypanosoma cruzi, an intracellular protozoan which is a potent stimulator of cell-mediated immunity. In the indeterminate form of CD (IFCD) a modulation between pro- and anti-inflammatory responses establishes a host-parasite adaptation. It was previously demonstrated that purinergic ecto-enzymes regulates extracellular ATP and adenosine levels, influencing immune and inflammatory processes during IFCD. In inflammatory sites ATP, as well as its degradation product, adenosine, function as signaling molecules and immunoregulators through the activation of purinergic receptors. In this work, it was analyzed the gene and protein expression of P2X7 purinergic receptor in peripheral lymphocytes and serum immunoregulatory cytokines from IFCD patients. Gene and protein expression of P2X7 receptor (P2X7R), and serum cytokines (IL-2, IL-10, IL-17 and IFN-γ) were unaltered. However, IFCD group showed significantly higher IL-4 and IL-6 levels while TNF-α was significantly decreased. These results indicate that imune profile of IFCD patients displays anti-inflammatory characteristics, consistent with the establishment of an immunomodulatory response. Further study about the molecular knowledge of P2X7R in IFCD is useful to clarify the participation of purinergic system in the regulatory mechanism which avoid the progression of CD.
恰加斯病（CD）由克氏锥虫引起，克氏锥虫是一种细胞内原生动物，是细胞介导免疫的强效刺激物。在CD的无症状感染期（IFCD），促炎反应和抗炎反应之间的调节建立了宿主与寄生虫的适应性。先前已证明，嘌呤能外切酶调节细胞外ATP和腺苷水平，影响IFCD期间的免疫和炎症过程。在炎症部位，ATP及其降解产物腺苷通过激活嘌呤能受体发挥信号分子和免疫调节剂的作用。在这项研究中，分析了IFCD患者外周淋巴细胞中P2X7嘌呤能受体的基因和蛋白表达以及血清免疫调节细胞因子。P2X7受体（P2X7R）的基因和蛋白表达以及血清细胞因子（IL-2、IL-10、IL-17和IFN-γ）未发生改变。然而，IFCD组的IL-4和IL-6水平显著升高，而TNF-α显著降低。这些结果表明，IFCD患者的免疫特征表现出抗炎特性，这与免疫调节反应的建立一致。进一步研究IFCD中P2X7R的分子知识，有助于阐明嘌呤能系统在避免CD进展的调节机制中的作用。
