Regulation of fish phagocytic functions by hormones and neurotransmitters

点击翻译按钮获取中文摘要

Plasma cortisol level of subordinate tilapia under social stress increased significantly, and neutrophil defense activities (respiratory burst and phagocytosis) from the subordinate fish were suppressed. Neutrophils incubated in a medium containing cortisol were impaired in their defense activities. From these results, cortisol could affect the neutrophil activities directly. Tissue-resident eosinophilic granular cells (EGCs), in which neutrophil-migrating factor (s) could be included, were also adversely affected in their degranulation by cortisol. Impaired EGC degranulating activity by cortisol could be involved in less migration of neutrophils to the inflammatory site under stressful conditions. These impaired non-specific defense mechanisms could increase susceptibility to infections and allow the infections to spread in the stressed fish. In fact, cortisol-implanted tilapia had higher susceptibility to Edwardosiella tarda infection.In contrast to cortisol, another stress hormone, β endorphin enhanced defense activities of head kidney phagocytes from rainbow trout in vivo and in vivo. Carp head kidney leucocytes also were stimulated by β endorphin in vitro. It is indicated that there are two types of stress hormones, phagocyte-inhibiting hormone and phagocyte-stimulating hormone.A neurotransmitter, adrenarin reduced the neutrophil defense activities in vitro. Adrenarin β receptor could be associated with this inhibition, with propranolol, antagonist of adrenarin β receptor, blocking the adverse effect of adrenarin on neutrophils. Serotonin, another neurotransmitter, also suppressed respirator burst of tilapia neutrophils in vitro. From these results, it is suggested that fish defense system is closely related with the nervous system.