Sánchez-Alemán Esperanza, Quintanar-Stephano Andrés, Escobedo Galileo, Campos-Esparza María del Rosario, Campos-Rodríguez Rafael, Ventura-Juárez Javier
Departamento de Morfología, Universidad Autónoma de Aguascalientes, Aguascalientes, Mexico.
Neuroimmunomodulation. 2015;22(3):166-80. doi: 10.1159/000362240. Epub 2014 May 6.
The parasympathetic nervous system modulates the immune response in the abdominal-pelvic gut through the vagus nerve, which releases acetylcholine. This endogenous ligand acts on α7 nicotinic receptors expressed on immune cells.
To study the mechanism of the production and regulation of cytokines in parasympathectomized and control hamsters during the development of amoebic liver abscesses (ALA) caused by Entamoeba histolytica.
Six- to 8-week-old male hamsters with and without vagotomy were used in a model of ALA. The animals were infected with trophozoites (350,000; HM1:IMSS strain) via the intrahepatic route and sacrificed at 6, 12, and 24 h and at 2, 4, and 7 days postinfection. Immune parameters were recorded at each time point using morphometric techniques including immunofluorescence and immunohistochemistry assays. These parameters included signal transducer and activator of transcription 3 (STAT3) levels, pro- and anti-inflammatory cytokine levels, and nuclear factor-κB (NFκB) activation in neutrophils and macrophages.
Compared to the control groups, the vagotomized (VAG) hamsters showed a significant increase in NFκB activation in neutrophils and macrophages, and higher levels of interleukin (IL)-1β, IL-6, interferon-γ, and tumor necrosis factor-α. VAG hamsters showed an increase in the expression of IL-8 and phosphorylated STAT3 during the first 24 h postinfection as well as slightly increased levels of transforming growth factor-β on days 2-7 postinfection. No significant differences were demonstrated in the levels of IL-10.
These results suggest that the vagus nerve plays an important role in the regulation of inflammation during ALA formation.
副交感神经系统通过释放乙酰胆碱的迷走神经调节腹盆腔肠道的免疫反应。这种内源性配体作用于免疫细胞上表达的α7烟碱受体。
研究在溶组织内阿米巴引起的阿米巴肝脓肿（ALA）形成过程中，去交感神经支配的仓鼠和对照仓鼠体内细胞因子产生和调节的机制。
6至8周龄的雄性仓鼠，分为迷走神经切断组和未切断组，用于ALA模型。动物通过肝内途径感染滋养体（350,000个；HM1:IMSS株），并在感染后6、12和24小时以及2、4和7天处死。使用形态计量技术（包括免疫荧光和免疫组织化学分析）在每个时间点记录免疫参数。这些参数包括信号转导和转录激活因子3（STAT3）水平、促炎和抗炎细胞因子水平以及中性粒细胞和巨噬细胞中核因子-κB（NFκB）的激活情况。
与对照组相比，迷走神经切断（VAG）的仓鼠中性粒细胞和巨噬细胞中的NFκB激活显著增加，白细胞介素（IL）-1β、IL-6、干扰素-γ和肿瘤坏死因子-α水平更高。VAG仓鼠在感染后最初24小时内IL-8和磷酸化STAT3的表达增加，在感染后第2至7天转化生长因子-β水平略有升高。IL-10水平未显示出显著差异。
这些结果表明迷走神经在ALA形成过程中的炎症调节中起重要作用。
