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首页> 外文期刊>Clinical and diagnostic laboratory immunology >Cytokine Gene Expression in Response to SnSAG1 in Horses with Equine Protozoal Myeloencephalitis
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Cytokine Gene Expression in Response to SnSAG1 in Horses with Equine Protozoal Myeloencephalitis

机译：马原生动物脊髓性脑炎马中细胞因子基因表达对SnSAG1的应答。

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Equine protozoal myeloencephalitis (EPM) is a neurologic syndrome seen in horses from the Americas and is mainly caused by Sarcocystis neurona. Recently, a 29-kDa surface antigen from S. neurona merozoites was identified as being highly immunodominant on a Western blot. This antigen has been sequenced and cloned, and the expressed protein has been named SnSAG1. In a previous study, cell-mediated immune responses to SnSAG1 were shown to be statistically significantly reduced in horses with EPM in comparison to EPM-negative control horses. It therefore appears as though the parasite is able to induce immunosuppression towards parasite-derived antigens as parasite-specific responses are decreased. Isolated peripheral blood lymphocytes from 21 EPM (cerebrospinal fluid [CSF] Western blot)-negative horses with no clinical signs and 21 horses with clinical signs of EPM (CSF Western blot positive) were cocultured with SnSAG1 for 48 and 72 h, and the effect on cytokine production was investigated by means of reverse transcriptase PCR. Cytokines assayed include gamma interferon (IFN-γ), tumor necrosis factor alpha, interleukin (IL)-2, IL-4, and IL-6. β-Actin was used as the housekeeping gene. A Wilcoxon signed-rank test of the findings indicated that there was a statistically significant decrease in IFN-γ production after 48 h in culture for samples from horses with clinical disease. There was also a statistically significant increase in IL-4 production after 72 h in culture for samples from horses with EPM. These results further support the notion that this parasite is able to subvert the immune system in horses with clinical disease.
机译：马原生动物脊髓性脑炎（EPM）是一种在美洲的马匹中看到的神经系统综合症，主要由 Sarcocystis neurona 引起。最近，来自 S的29-kDa表面抗原。在蛋白质印迹中，神经元裂殖子被确认为高度免疫优势。该抗原已测序并克隆，表达的蛋白质已命名为SnSAG1。在先前的研究中，与EPM阴性对照马匹相比，具有EPM的马匹对SnSAG1的细胞介导的免疫反应在统计学上显着降低。因此，随着寄生虫特异性应答的降低，似乎该寄生虫能够诱导针对寄生虫来源的抗原的免疫抑制。将无临床体征的21例EPM（脑脊液[CSF] Western blot）阴性马和21例具有EPM的临床体征（CSF Western blot阳性）马分离的外周血淋巴细胞与SnSAG1共培养48和72 h。通过逆转录酶PCR研究细胞因子的产生。检测的细胞因子包括γ干扰素（IFN-γ），肿瘤坏死因子α，白介素（IL）-2，IL-4和IL-6。 β-肌动蛋白被用作管家基因。对发现的Wilcoxon秩次检验表明，对于患有临床疾病的马，培养48小时后，IFN-γ的产生在统计学上显着降低。在培养72小时后，带有EPM的马的样品中IL-4的产生也有统计上的显着增加。这些结果进一步支持了这种寄生虫能够破坏患有临床疾病的马的免疫系统的观点。

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