β-Glucan-induced cortisol levels improve the early immune response in matrinxã (Brycon amazonicus) - PubMed (original) (raw)
β-Glucan-induced cortisol levels improve the early immune response in matrinxã (Brycon amazonicus)
Luz N Franco Montoya et al. Fish Shellfish Immunol. 2017 Jan.
Abstract
This study investigated the role of endogenous cortisol on the innate immune response in matrinxã (Brycon amazonicus) fed with β-glucan, prior to and after stressor exposure and bacterial challenge. For this, we evaluated the serum cortisol and plasma glucose levels, the serum lysozyme levels, the hemolytic activity of the complement system, and the respiratory activity of leukocytes, as well as the number of circulating erythrocytes and leukocytes of fish fed during 15 days with diets containing β-glucan 0.1% (β-G) or β-glucan 0.1% + metyrapone 30 mg kg-1 fish (β-G + MTP). Dietary MTP was used to block cortisol production. After feeding, fish were air-exposed during 3 min, to endogenously increase the cortisol levels. Following that, they were challenged with intraperitoneal injection of Aeromonas hydrophila. Results were compared with a positive control group fed with a β-glucan-free diet. A negative control group, also fed with β-glucan-free diet but inoculated with PBS, was established to evaluate the effect of the handling during injection. Fish were sampled prior to the stressor exposure, 30 min after exposure, and 24 h post infection (hpi). Herein we observed that dietary β-G modulated the cortisol profile prior to and after the stressor, increasing the number and activity of leukocytes. Moreover, cortisol showed to be an efficient modulator of both humoral and cellular innate immune system by increasing lysozyme and complement activity, as well as neutrophil and monocyte populations. Our results suggest that β-glucan-induced cortisol increase is one important mechanism to improve the innate immune response in matrinxã.
Keywords: Acute infection; Acute stress; Capture; Early immune defense; Handling.
Copyright © 2016 Elsevier Ltd. All rights reserved.
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