灭活柱状黄杆菌浸泡免疫诱导草鱼中pIgR和四种细胞因子免疫应答特性的研究

Characterization of pIgR and four cytokines immune response in Ctenopharyngodon idellus after Flavobacterium columnare bathing

多聚免疫球蛋白受体(pIgR)通过介导分泌型免疫球蛋白的转运,进而发挥黏膜防御功能,而细胞因子TNFα、IFNγ、IL-1β和IL-4对pIgR表达具有调节作用。本试验采用实时荧光定量PCR(qPCR)技术检测了灭活柱状黄杆菌浸泡免疫诱导草鱼(Ctenopharyngodon idellus)各组织中pIgR及TNFα、IFNγ、IL-1β和IL-4基因的免疫应答特性。结果显示:浸泡免疫柱状黄杆菌可诱导草鱼中pIgR和4种细胞因子发生显著上调表达;pIgR和4种细胞因子的上调表达趋势相似,均在96 h内呈现先上升后下降趋势;其中对黏膜免疫组织皮肤和鳃中的pIgR和4种细胞因子的表达影响较大,显著上调达到峰值的时间短且峰值高,峰值分别为对照组的2.83~56.62倍和2.75~36.25倍;而系统免疫组织脾、头肾中的pIgR和4种细胞因子表达量到达峰值时间较晚,峰值分别为对照组的3.11~46.07倍和1.91~17.4倍;肠和肝中pIgR和4种细胞因子表达量峰值分别为对照组的2.43~9.26倍和2.21~24.13倍。本文研究结果为进一步探究TNFα、IFNγ、IL-1β和IL-4对草鱼pIgR的表达调节提供了数据支撑。

The polymeric immunoglobulin receptor(pIgR) plays an important role in mediating the transcytosis of polymeric immunoglobulins to protect the organisms against pathogens invading while the cytokines TNF α, IFN γ, IL-1β and IL-4 regulate the synthesis of pIgR. In this study, by quantitative real time polymerase chain reaction(qPCR), the expression changes of pIgR, TNF α, IFN γ, IL-1β and IL-4 were detected in the tissues of Ctenopharyngodon idellus after immunization bathing with Flavobacterium columnare. The results revealed that the expressions of pIgR, TNF α, IFN γ, IL-1β and IL-4 were all up-regulated significantly by immersion immunization. The expression of the five genes first increased and then decreased within 96 hours.Immersion immunization had a greater influence on the expression of genes in the mucosal immune tissues(skin and gills). The expression of five genes reached the peak in a short time in these two tissues, being 2.83-56.62 folds and 2.75-36.25 folds of the control. On the other hand, the expression of pIgR and four cytokines in the systemic immune tissues(spleen and head kidney) reached the peak later, being 3.11-46.07 folds and 1.91-17.4 folds of the control, respectively. The peak abundances of five genes varied between 2.83 and 56.62 folds and between 2.75 and 36.25 folds of the control in intestine and liver. In conclusion, our findings provided data supporting further studying on the regulation of pIgR gene expression by the cytokines TNF α, IFN γ, IL-1β and IL-4.