The Direct Exposure of Cortisol Does Not Modulate the Expression of Immune-Related Genes on Tissue Explants of Mucosal Surfaces in Rainbow Trout (Oncorhynchus mykiss) Nor in Gilthead Sea Bream (Sparus aurata)

Eva Vallejos-Vidal,Joan Carles Balasch,Felipe E Reyes-López,Ali Reza Khansari,Lluc Soliva-Dueso,Lluis Tort

doi:10.3389/fmars.2022.828050

Abstract

The stress response in fish is characterized by the activation of the HPI axis resulting in the release of cortisol. Previous studies in rainbow trout (Oncorhynchus mykiss) and gilthead sea bream (Sparus aurata) have shown that an acute stressor modulates the expression of immune- and stress-related genes in mucosal-associated lymphoid tissues (MALTs), particularly in the skin (SALT), gills (GIALT), and gut (GALT). However, there are no antecedents on whether the modulation on the mucosal transcriptomic profile is coordinated through the local presence of cortisol in the mucosal tissue surface. Thus, the aim of this study was to evaluate the effect of cortisol upon the modulation of a set of immune- (il-1β, il-6, tnf-α, and cox-2) and stress-related (hsp70, gr1) genes. For this purpose, tissue explants cultures were incubated with cortisol (100 ng/100 mg tissue) for 2-, 4-, and 24 h and the gene expression profile was evaluated at each time-point by real-time PCR. No differences were found in the gene expression between cortisol-incubated tissue explants and mock-incubated tissues in any of the time-points tested for both species. These results suggest that the quick modulation of the gene expression during the first 24 h after the exposure to stressor challenge reported in previous studies, is probably coordinated and mediated through a systemic-dependent mechanism but not through a peripheral/local response on mucosal tissue surfaces.

Highlights

The stress response is a physiological complex mechanism activated by a stimulus that is perceived by the organism as a potential threat (Tort, 2011)
The HPI axis activation is responsible for the synthesis of hypothalamic corticotrophin-releasing hormone (CRH) from the hypothalamic paraventricular nucleus (PVN), which in turn promotes the secretion of adrenocorticotropic hormone (ACTH) by the pituitary gland (Khansari et al, 2017a)
Our results clearly show that cortisol by itself does not significantly modulate the expression of the genes evaluated in mucosal surfaces of either rainbow trout and gilthead sea bream at any of the time-points tested (2, 4, and 24 h post-incubation) compared to the mock-incubated group

Summary

Introduction

The stress response is a physiological complex mechanism activated by a stimulus that is perceived by the organism as a potential threat (Tort, 2011) It involves a sum of sequential and coordinated activation mechanisms at different functional levels including molecular processes with direct repercussions on gene expression and protein synthesis that, at the end, will activate the responses from cellular to systemic and performance levels (Parra et al, 2015). The SAM axis is characterized by the neuronal signaling to secrete catecholamines (adrenaline and noradrenaline) by chromaffin cells. This response is known as the fight-or-flight reaction and it takes place in a matter of seconds to a few minutes (Schreck and Tort, 2016). The ACTH is recognized by the melanocortin receptor 2 (MC2R) of the interrenal cells, activating the steroidogenic signaling pathway responsible for cortisol synthesis

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