Abstract
Tetracapsuloides bryosalmonae Canning et al., 1999 (Myxozoa) is the causative agent of proliferative kidney disease in various species of salmonids in Europe and North America. We have shown previously that the development and distribution of the European strain of T. bryosalmonae differs in the kidney of brown trout (Salmo trutta) Linnaeus, 1758 and rainbow trout (Oncorhynchus mykiss) Walbaum, 1792, and that intra-luminal sporogonic stages were found in brown trout but not in rainbow trout. We have now compared transcriptomes from kidneys of brown trout and rainbow trout infected with T. bryosalmonae using suppressive subtractive hybridization (SSH). The differentially expressed transcripts produced by SSH were cloned, transformed, and tested by colony PCR. Differential expression screening of PCR products was validated using dot blot, and positive clones having different signal intensities were sequenced. Differential screening and a subsequent NCBI-BLAST analysis of expressed sequence tags revealed nine clones expressed differently between both fish species. These differentially expressed genes were validated by quantitative real-time PCR of kidney samples from both fish species at different time points of infection. Expression of anti-inflammatory (TSC22 domain family protein 3) and cell proliferation (Prothymin alpha) genes were upregulated significantly in brown trout but downregulated in rainbow trout. The expression of humoral immune response (immunoglobulin mu) and endocytic pathway (Ras-related protein Rab-11b) genes were significantly upregulated in rainbow trout but downregulated in brown trout. This study suggests that differential expression of host anti-inflammatory, humoral immune and endocytic pathway responses, cell proliferation, and cell growth processes do not inhibit the development of intra-luminal sporogonic stages of the European strain of T. bryosalmonae in brown trout but may suppress it in rainbow trout.
Highlights
Proliferative kidney disease (PKD) significantly affects both farmed and wild salmonid fish in Europe and North America, causes economic losses, and endangers wild fish populations (El-Matbouli and Hoffmann 2002; Okamura et al 2011)
Previous studies have examined innate and adaptive immune genes such as inflammatory, antimicrobial, macrophage, antibody, and T helper cell marker genes in rainbow trout infected with European strain of T. bryosalmonae (Holland et al 2003; Gorgoglione et al 2013), but very little is known about gene expression in brown trout (Kumar et al 2014)
We report the first gene expression study of suppressive subtractive hybridization (SSH) identified genes in the kidney of brown trout and rainbow trout infected with the European strain of T. bryosalmonae at different time points
Summary
Proliferative kidney disease (PKD) significantly affects both farmed and wild salmonid fish in Europe and North America, causes economic losses, and endangers wild fish populations (El-Matbouli and Hoffmann 2002; Okamura et al 2011). In North America, rainbow trout can Parasitol Res (2015) 114:929–939 form spores in kidney tubules (Kent and Hedrick 1986; Hedrick et al 2004). This led to the hypothesis that there are two lineages of T. bryosalmonae: one adapted to the genus Salmo and the other to the genus Oncorhynchus (Bucke et al 1991; Morris et al 1997). Grabner and El-Matbouli (2008) and Kumar et al (2013) showed that rainbow trout infected with European strain of T. bryosalmonae could not transmit the parasite to bryozoan Fredericella sultana Blumenbach, 1779, but infected brown trout could. We verified the persistence of T. bryosalmonae in chronically infected brown trout and their ability to infect the bryozoan colonies up to 104 weeks post-exposure (wpe) (Abd-Elfattah et al 2014)
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