The Roslin Institute &R(D)SVS, University of Edinburgh, Easter Bush, Midlothian EH25 9RG. U.K.
Moredun Research Institute, International Research Centre, Pentlands Science Park, Penicuik, Midlothian EH26 0PZ, UK.
Sci Rep. 2017 Apr 24;7:46695. doi: 10.1038/srep46695.
Multibacillary and paucibacillary paratuberculosis are both caused by Mycobacterium avium subspecies paratuberculosis. Multibacillary lesions are composed largely of infected epithelioid macrophages and paucibacillary lesions contain T cells but few bacteria. Multibacillary disease is similar to human lepromatous leprosy, with variable/high levels of antibody and a dysfunctional immune response. Animals with paucibacillary disease have high cell-mediated immunity and variable levels of antibody. This study aims to characterize the immunological dysfunction using TruSeq analysis of the ileocaecal lymph node that drains disease lesions. Immune dysfunction is highlighted by repression of TCR/CD3 genes, T cell co-receptors/co-stimulators, T cell activation and signal-transduction genes. Inflammation was an acute phase response and chronic inflammation, with little evidence of acute inflammation. The high levels of immunoglobulin and plasma cell transcripts is consistent with the anti-MAP antibody responses in paratuberculosis sheep. Also notable was the overwhelming reduction in mast cell transcripts, potentially affecting DC activation of the immune response. This study also shows that there were no fundamental differences in the gene expression patterns in multibacillary and paucibacillary disease, no shift in T cell genes from Th1 to Th2 pattern but rather an incremental decline into immune dysfunction leading to multibacillary pathology.
分枝杆菌病和少菌型分枝杆菌病均由鸟分枝杆菌亚种副结核分枝杆菌引起。多菌型病变主要由感染的上皮样巨噬细胞组成,少菌型病变含有 T 细胞但细菌很少。多菌型疾病类似于人类瘤型麻风病,具有可变/高水平的抗体和功能失调的免疫反应。少菌型疾病动物具有高细胞介导的免疫力和可变水平的抗体。本研究旨在通过分析引流病变的回盲淋巴结的 TruSeq 来描述免疫功能障碍。免疫功能障碍的特点是 TCR/CD3 基因、T 细胞共受体/共刺激物、T 细胞激活和信号转导基因的抑制。炎症是急性期反应和慢性炎症,几乎没有急性炎症的证据。高水平的免疫球蛋白和浆细胞转录本与副结核病绵羊中的抗-MAP 抗体反应一致。值得注意的是,肥大细胞转录本大量减少,可能影响 DC 对免疫反应的激活。本研究还表明,多菌型和少菌型疾病的基因表达模式没有根本差异,T 细胞基因没有从 Th1 向 Th2 模式转移,而是逐渐出现免疫功能障碍,导致多菌型病变。