Institute of Marine Research, P.O. Box 1870, Nordnes, 5817, Bergen, Norway.
Uni Research Environment, Uni Research, NORCE, Nygårdsgaten 112, 5006, Bergen, Norway.
Fish Shellfish Immunol. 2018 Nov;82:579-590. doi: 10.1016/j.fsi.2018.08.059. Epub 2018 Aug 31.
Salmonid alphavirus (SAV) causes pancreas disease (PD) in Atlantic salmon (Salmo salar L.) and disease outbreaks are mainly detected after seawater transfer. The influence of the smoltification process on the immune responses, specifically the adaptive response of Atlantic salmon after SAV infection, is not fully understood. In this study, Atlantic salmon post-smolts were infected by either bath immersion (BI) or intramuscular injection (IM) with SAV subtype 3, 2 weeks (Phase A) or 9 weeks (Phase B) after seawater transfer. The transcript levels of genes related to cellular, humoral and inflammatory responses were evaluated on head kidney samples collected at 3, 7, 14, 21, and 28 days post-infection (dpi). Corresponding negative control groups (CT) were established accordingly. Significant differences were found between both phases and between the IM and BI groups. The anti-inflammatory cytokine IL-10 was up-regulated in Phase A at a higher level than in Phase B. High mRNA levels of the genes RIG-1, SOCS1 and STAT1 were observed in all groups except the BI-B group (BI-Phase B). Moreover, the IM-B group showed a higher regulation of genes related to cellular responses, such as CD40, MHCII, and IL-15, that indicated the activation of a strong cell-mediated immune response. CD40 mRNA levels were elevated one week earlier in the BI-B group than in the BI-A group (BI-Phase A). A significant up-regulation of IgM and IgT genes was seen in both IM groups, but the presence of neutralizing antibodies to SAV was detected only in Phase B fish at 21 and 28 dpi. In addition, we found differences in the basal levels of some of the analysed genes between non-infected control groups of both phases. Findings suggest that Atlantic salmon post-smolts adapted for a longer time to seawater before they come into contact with SAV, developed a stronger humoral and cell-mediated immune response during a SAV infection.
鲑鱼甲肝病毒(SAV)可引起大西洋鲑鱼的胰腺病(PD),该病的爆发主要发生在海水转移后。人们对变态过程对免疫反应的影响,特别是大西洋鲑鱼在 SAV 感染后的适应性反应,还不完全了解。在这项研究中,大西洋鲑鱼幼鱼在海水转移后 2 周(A 期)或 9 周(B 期),通过浸浴(BI)或肌肉注射(IM)感染 SAV 亚 3 型。在感染后第 3、7、14、21 和 28 天采集头肾样本,评估与细胞、体液和炎症反应相关的基因的转录水平。相应地建立了阴性对照组(CT)。在两个阶段和 IM 与 BI 组之间均发现了显著差异。在 A 期,抗炎细胞因子 IL-10 的上调水平高于 B 期。在所有组中,除 BI-B 组(BI-Phase B)外,均观察到 RIG-1、SOCS1 和 STAT1 基因的高 mRNA 水平。此外,IM-B 组表现出与细胞反应相关基因的更高调节,例如 CD40、MHCII 和 IL-15,表明细胞介导的免疫反应强烈激活。BI-B 组的 CD40mRNA 水平比 BI-A 组早一周升高。在两个 IM 组中均观察到 IgM 和 IgT 基因的显著上调,但仅在 B 期鱼中在 21 和 28dpi 时检测到针对 SAV 的中和抗体。此外,我们发现两个阶段的非感染对照组之间的一些分析基因的基础水平存在差异。研究结果表明,大西洋鲑鱼幼鱼在接触 SAV 之前,需要更长的时间来适应海水,在 SAV 感染期间,它们发展出更强的体液和细胞介导的免疫反应。