Development of adaptive immunity in rainbow trout, Oncorhynchus mykiss (Walbaum) surviving an infection with Yersinia ruckeri

Abstract

Development of adaptive immunity in rainbow trout ( Oncorhynchus mykiss) surviving a primary infection with 5 × 10 5 CFU Yersinia ruckeri O1 (LD 50 dose) was investigated by transcriptome analysis of spleen tissue. These fish surviving a primary infection showed also a significantly increased survival following a secondary infection (same dose) when compared to naïve trout. The weight of the rainbow trout spleen doubled during the first 14 days of the primary infection but the affected organs subsequently recovered normal weight which remained constant during the re-infection period. Gene transcription in the spleen was measured using Quantitative real-time RT-PCR (qPCR). Samples taken 8 h.p.i., 1, 3, 7, 14 and 28 d.p.i. were compared to PBS-injected control fish sampled at the same time points. The investigated cytokines and chemokines comprised interleukin (IL)-1β, IL-1 receptor antagonist (Ra), IL-6, IL-8, IL-10, IL-11 and IFN-γ, IL-1 receptor I and II (IL-RI and IL-RII). Transcript levels of genes encoding cytokines and receptors were increased during the primary infection but not during the secondary infection. Changes of T cell occurrence or activity in the spleen during the infections were inferred from the transcript level of T cell receptor (TCR), CD4 and CD8α genes. No alteration in the expression of MHC class ll and immunoglobulin (Ig)M and IgT was detected during the experiment. The amount of Y. ruckeri O1 in the spleen was measured with a Y. ruckeri 16S ribosomal RNA specific qPCR and this parameter was correlated to the expression of IL-1β, IL-8 and IL-10 genes with a peak expression at 3 d.p.i. (first infection). The low transcript levels of the bacterial gene and the hosts' immune genes during the re-infection can be interpreted as a result of development of adaptive immunity. This would explain the relatively fast elimination of the bacteria during the secondary infection whereby the activation of cytokines becomes less pronounced.