The serum proteome of Atlantic salmon, Salmo salar, during pancreas disease (PD) following infection with salmonid alphavirus subtype 3 (SAV3)

Abstract

Salmonid alphavirus is the aetological agent of pancreas disease (PD) in marine Atlantic salmon, Salmo salar, and rainbow trout, Oncorhynchus mykiss, with most outbreaks in Norway caused by SAV subtype 3 (SAV3). This atypical alphavirus is transmitted horizontally causing a significant economic impact on the aquaculture industry. This histopathological and proteomic study, using an established cohabitational experimental model, investigated the correlation between tissue damage during PD and a number of serum proteins associated with these pathologies in Atlantic salmon. The proteins were identified by two-dimensional electrophoresis, trypsin digest and peptide MS/MS fingerprinting. A number of humoral components of immunity which may act as biomarkers of the disease were also identified. For example, creatine kinase, enolase and malate dehydrogenase serum concentrations were shown to correlate with pathology during PD. In contrast, hemopexin, transferrin, and apolipoprotein, amongst others, altered during later stages of the disease and did not correlate with tissue pathologies. This approach has given new insight into not only PD but also fish disease as a whole, by characterisation of the protein response to infection, through pathological processes to tissue recovery.Biological significanceSalmonid alphavirus causes pancreas disease (PD) in Atlantic salmon, Salmo salar, and has a major economic impact on the aquaculture industry. A proteomic investigation of the change to the serum proteome during PD has been made with an established experimental model of the disease. Serum proteins were identified by two-dimensional electrophoresis, trypsin digest and peptide MS/MS fingerprinting with 72 protein spots being shown to alter significantly over the 12 week period of the infection. The concentrations of certain proteins in serum such as creatine kinase, enolase and malate dehydrogenase were shown to correlate with tissue pathology while other proteins such as hemopexin, transferrin, and apolipoprotein, altered in concentration during later stages of the disease and did not correlate with tissue pathologies. The protein response to infection may be used to monitor disease progression and enhance understanding of the pathology of PD.

Identification of a warm‐temperature acclimation‐associated 65‐kDa protein encoded by a temperature‐ and infection‐responsive gene in the Kumgang fat minnow Rhynchocypris kumgangensis

“…In particular, hemopexin expression is up‐regulated by pro‐inflammatory cytokines (Diaz‐Rosales et al, ). As noted above, teleost Wap65 expression is also increased by inflammation caused by viruses and bacteria (Braceland et al, ). Taken together, these observations suggest that Wap65 up‐regulation might serve to clear inflammation‐associated free heme.…”

Comparative pathogenesis of piscirickettsiosis in Atlantic salmon (Salmo salar L.) post‐smolt experimentally challenged with LF‐89‐like and EM‐90‐like Piscirickettsia salmonis isolates

“…The decrease in the level of TOP and ALB in fish infected by P. salmonis could be explained by a reduction in protein synthesis due to liver damage and by the higher excretion of protein or protein loss associated with kidney damage. Protein synthesis can decrease during infection due to preferential synthesis of specific proteins, and albumin may act as an acute‐phase negative protein (Braceland et al., ). These results agree with reports in tilapia, Oreochromis sp.…”

Proteomic analysis of anatoxin-a acute toxicity in zebrafish reveals gender specific responses and additional mechanisms of cell stress

“…The contrasting abundances of the two muscle eno1 isoforms may indicate a turn-over of activity controlled by post-translational modification. Eno1 has been regarded as a marker of stress and disease (Braceland et al, 2013;Cordeiro et al, 2012;Wozny et al, 2012). Eno1 has been also considered an important neurotrophic factor and is under the transcriptional regulation of a number of stimuli, such as ischemia, hypoxia, cytokines and mitogens (Li et al, 2014;Sousa et al, 2005).…”