Effects of cortisol on innate immune responses and on mRNA levels of corticosteroid receptors in rainbow trout

Abstract

Cortisol is a key hormone in the fish stress response with a well known ability to regulate several physiological functions, including carbohydrate metabolism and the immune system. The consequences of cortisol actions in tissues are performed through the corticosteroid receptors (CRs) that have been characterized in fish during the last years. However, data concerning cortisol effects on fish innate immune system and on the transcriptional pattern of the CRs using a more controlled increase in cortisol levels isolated from any other stress related signaling is scarce. Keeping in mind the previous findings, in the present study we injected rainbow trout with slow-release cortisol implants to create medium to high levels of circulating cortisol over extended time periods emulating an acute to chronic stress. Ten days after implantation the cortisol levels in plasma returned to control levels, emulating the period of fish recovery after stress. Glucose and lactate were also returned to control levels corroborating the recovery of the fish after cortisol injection. Thus, the present research work describes the effect of cortisol on selected innate immune responses, such as lysozyme and complement (ACH50) activities, during the recovery period. The mRNA levels of lysozyme and complement C3, factor H and factor B were measured in liver. Furthermore, we present the results concerning the transcriptional levels of the CRs in several organs of trout after 10 days implantation. The results revealed that when plasma cortisol returned to basal levels, lysozyme and ACH50 activities were significantly decreased. These results reflect a latter down-regulatory effect of cortisol on the activity of both ACH50 and lysozyme, which is in agreement with previous findings in stressed fish. In the liver, the mRNA levels of lysozyme, factor B and factor H were also significantly decreased in the recovery period. These changes in mRNA abundances correlate with the plasma data, since both lysozyme and complement activities decreased. Thus, these results suggest that cortisol regulates the expression of lysozyme and complement factors in the liver and that this effect would possibly lead to reduced plasma lysozyme and ACH50 activities. Overall, results support the relevant role of cortisol in modulating key components of the innate immune response in fish, such lysozyme or ACH50 activities, and the expression of their related genes. We also show that even in the recovery period we still found changes in the transcriptional levels of the CRs in gills, spleen and gonads.