Benedicenti Ottavia, Collins Catherine, Wang Tiehui, McCarthy Una, Secombes Christopher J
Scottish Fish Immunology Research Centre, Institute of Biological and Environmental Sciences, University of Aberdeen, Tillydrone Avenue, Aberdeen AB24 2TZ, UK; Marine Scotland Science Marine Laboratory, 375 Victoria Rd, Aberdeen AB11 9DB, UK.
Marine Scotland Science Marine Laboratory, 375 Victoria Rd, Aberdeen AB11 9DB, UK.
Fish Shellfish Immunol. 2015 Oct;46(2):417-25. doi: 10.1016/j.fsi.2015.07.002. Epub 2015 Jul 9.
Amoebic gill disease (AGD) is an emerging disease in North European Atlantic salmon (Salmo salar Linnaeus 1758) aquaculture caused by the amoeba Paramoeba perurans. The host immune response to AGD infection is still not well understood despite past attempts to investigate host-pathogen interactions. With the significant increase in our knowledge of cytokine genes potentially involved in Th responses in recent years, we examined their involvement in this disease using Atlantic salmon post-smolts sampled 3 weeks after exposure to either 500 or 5000 cells/l P. perurans. Gene expression analysis of cytokines potentially involved in the different Th pathways was performed on the first gill arch including the interbranchial lymphoid tissue (ILT). Th1, Th17 and Treg pathways were found to be significantly down regulated, mainly in samples from fish given the higher dose. In contrast, the Th2 pathway was found to be significantly up regulated by both infection doses. Correlation analysis of the gene expression data and the P. perurans load, assessed by real time RT-PCR of the 18S rRNA, was also performed. In humans, Th2 driven responses are characterized by the production of IgE, which in the majority of worm infections results in the generation of a Th2-mediated response and directs the immune system away from a Th1 inflammatory response. The present results seen during late stage AGD suggest that either an immune evasion strategy, similar to the responses driven by helminthic parasites to avoid cell-mediated killing mechanisms, or an allergic reaction caused by the parasite, is occurring.
阿米巴鳃病（AGD）是北欧大西洋鲑（Salmo salar Linnaeus 1758）水产养殖中出现的一种疾病，由阿米巴原虫Paramoeba perurans引起。尽管过去曾尝试研究宿主与病原体的相互作用，但宿主对AGD感染的免疫反应仍未得到很好的理解。近年来，随着我们对可能参与Th反应的细胞因子基因的了解大幅增加，我们使用暴露于500或5000个细胞/升秘鲁副变形虫3周后的大西洋鲑后幼鱼，研究了它们在这种疾病中的作用。对包括鳃间淋巴组织（ILT）的第一鳃弓进行了可能参与不同Th途径的细胞因子的基因表达分析。发现Th1、Th17和Treg途径显著下调，主要在给予较高剂量的鱼的样本中。相比之下，发现Th2途径在两种感染剂量下均显著上调。还对基因表达数据与通过18S rRNA实时RT-PCR评估的秘鲁副变形虫负荷进行了相关性分析。在人类中，Th2驱动的反应以IgE的产生为特征，在大多数蠕虫感染中，这会导致Th2介导的反应产生，并使免疫系统远离Th1炎症反应。在AGD晚期观察到的目前结果表明，要么是一种免疫逃避策略，类似于由蠕虫寄生虫驱动的反应以避免细胞介导的杀伤机制，要么是由寄生虫引起的过敏反应正在发生。
