Abstract
Chronic stress is a major factor in the poor growth and immune performance of salmonids in aquaculture. However, the molecular mechanisms linking stress effects to growth and immune dysfunction is poorly understood. The suppressors of cytokine signaling (SOCS), a family of genes involved in the inhibition of JAK/STAT pathway, negatively regulates growth hormone and cytokine signaling, but their role in fish is unclear. Here we tested the hypothesis that cortisol modulation of SOCS gene expression is a key molecular mechanism leading to growth and immune suppression in response to stress in fish. Exposure of rainbow trout (Oncorhynchus mykiss) liver slices to cortisol, mimicking stress level, upregulated SOCS-1 and SOCS-2 mRNA abundance and this response was abolished by the glucocorticoid receptor antagonist mifepristone. Bioinformatics analysis confirmed the presence of putative glucocorticoid response elements in rainbow trout SOCS-1 and SOCS-2 promoters. Prior cortisol treatment suppressed acute growth hormone (GH)-stimulated IGF-1 mRNA abundance in trout liver and this involved a reduction in STAT5 phosphorylation and lower total JAK2 protein expression. Prior cortisol treatment also suppressed lipopolysaccharide (LPS)-induced IL-6 but not IL-8 transcript levels; the former but not the latter cytokine expression is via JAK/STAT phosphorylation. LPS treatment reduced GH signaling, but this was associated with the downregulation of GH receptors and not due to the upregulation of SOCS transcript levels by this endotoxin. Collectively, our results suggest that upregulation of SOCS-1 and SOCS-2 transcript levels by cortisol, and the associated reduction in JAK/STAT signaling pathway, may be a novel mechanism leading to growth reduction and immune suppression during stress in trout.
Highlights
Plasma corticosteroid elevation is a highly conserved response to stressor exposure in vertebrates, and is essential to adapting animals to stress and overcoming the stressor [1]
We propose a novel mechanism by which cortisol signaling may curtail energy demanding growth and inflammatory responses during stress in fish
Stressed levels of cortisol upregulates suppressors of cytokine signaling (SOCS)-1 and SOCS-2 transcript levels and these are mediated by glucocorticoid receptor (GR) activation in trout liver
Summary
Plasma corticosteroid elevation is a highly conserved response to stressor exposure in vertebrates, and is essential to adapting animals to stress and overcoming the stressor [1]. Coping with stress is energy demanding and elevated corticosteroid levels increase the metabolic rate and energy substrate mobilization in animals [2]. Exposure to stressors, including handling for grading, crowding and transportation, are part and parcel of aquaculture operations [3]. These hatchery practices lead to reduced growth and increased disease susceptibility, resulting in an overall decrease in fish production [4]. The link between stressor exposure and the effects on growth and immune functions are far from clear
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