Bridle Andrew R, Morrison Richard N, Nowak Barbara F
School of Aquaculture, Tasmanian Aquaculture and Fisheries Institute and Aquafin CRC, University of Tasmania, Locked Bag 1370, Launceston 7250, Tasmania, Australia.
Fish Shellfish Immunol. 2006 Mar;20(3):346-64. doi: 10.1016/j.fsi.2005.05.014.
Amoebic gill disease (AGD) is an ectoparasitic disease caused by infection with the protozoan Neoparamoeba sp. and is characterised by epithelial hyperplasia that manifests as gill lesions. In order to examine the nature of the immune response to AGD, the expression of a range of immune-regulatory genes was examined in naïve uninfected rainbow trout, Oncorhynchus mykiss, and naïve rainbow trout subjected to a laboratory-induced AGD infection. The immune-regulatory genes examined were interleukin-1 beta isoform 1 (IL-1beta1), tumour necrosis factor alpha isoforms 1 and 2 (TNF-alpha1, TNF-alpha2), interleukin-8 (IL-8), transforming growth factor beta isoform 1 (TGF-beta1), inducible nitric oxide synthase (iNOS), cyclooxygenase 2 (COX-2), major histocompatibility complex beta chain (MHC-II beta-chain) and T-cell receptor beta chain (TCR beta-chain). Immune-regulatory genes that were up/down-regulated in AGD-infected trout compared to uninfected controls at 0, 7, and 14 days post-inoculation (p.i.) in gill, liver and anterior kidney tissue were initially identified by means of semi-quantitative RT-PCR. Up/down-regulated immune-regulatory genes were subsequently quantitated and validated by real-time RT-PCR (qRT-PCR). The extent of AGD-associated pathology was consistent amongst all AGD-infected trout at 7 days p.i. and increased considerably by 14 days p.i. At both 7 and 14 days p.i. IL-1beta1 and iNOS gene expression was significantly up-regulated in the gills, and IL-8 was significantly up-regulated in the liver of AGD-infected trout at 7 days p.i. These data demonstrate the involvement of the immune response to AGD at the molecular level, and indicate the importance of this response at the site of infection and the possible involvement of a systemic immune response.
阿米巴鳃病（AGD）是一种由原生动物新帕拉变形虫属感染引起的外寄生虫病，其特征是上皮细胞增生，表现为鳃部病变。为了研究对AGD免疫反应的本质，在未感染的幼稚虹鳟鱼（Oncorhynchus mykiss）以及经实验室诱导感染AGD的幼稚虹鳟鱼中，检测了一系列免疫调节基因的表达。所检测的免疫调节基因包括白细胞介素-1β亚型1（IL-1β1）、肿瘤坏死因子α亚型1和2（TNF-α1、TNF-α2）、白细胞介素-8（IL-8）、转化生长因子β亚型1（TGF-β1）、诱导型一氧化氮合酶（iNOS）、环氧化酶2（COX-2）、主要组织相容性复合体β链（MHC-IIβ链）和T细胞受体β链（TCRβ链）。通过半定量逆转录聚合酶链反应（RT-PCR）初步鉴定了在接种后0、7和14天，与未感染对照组相比，AGD感染鳟鱼的鳃、肝脏和前肾组织中上调/下调的免疫调节基因。随后通过实时RT-PCR（qRT-PCR）对上调/下调的免疫调节基因进行定量和验证。在接种后7天，所有AGD感染的鳟鱼中AGD相关病理程度一致，到接种后14天显著增加。在接种后7天和14天，AGD感染鳟鱼的鳃中IL-1β1和iNOS基因表达显著上调，在接种后7天，AGD感染鳟鱼的肝脏中IL-8显著上调。这些数据证明了在分子水平上对AGD免疫反应的参与，并表明了这种反应在感染部位的重要性以及全身免疫反应的可能参与。
