Neural regulation of immunity in teleosts Public Deposited

http://ir.library.oregonstate.edu/concern/graduate_thesis_or_dissertations/qz20sw19x

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  • It has long been observed that stress can increase our susceptibility to infectious diseases and cancers. Recent experimental evidence suggests that this increased susceptibility is due to suppression of immunity. A variety of neuroendocrine products are released during periods of stress, and a large number of these are now known to influence leukocyte function via a receptor mediated process. Indeed, the capacity for neural and hormonal regulation of immunity in mammals is now well established. Direct neural control of immune reactivity is evidenced by the extensive autonomic innervation of lymphoid tissues, the effects of denervation on immunity, the presence of high affinity receptors for autonomic neurotransmitters on leukocyte membranes, and the multitude of leukocyte functions which can be altered by adrenergic and cholinergic agents in vitro. This thesis demonstrates that the immune systems of certain teleosts are also susceptible to some degree of neural control. The spleen of the coho salmon, Oncorhynchus kisutch, contains a rich adrenergic innervation. Depletion of peripheral catecholamine stores with 6-hydroxydopamine (6 -OHDA) resulted in an increased number of antibody-secreting cells in the spleens of subsequently immunized fish. 6 -OHDA treatment did not influence plasma cortisol levels, and did not affect the antibody response if administered one week after, rather than two days prior to, immunization. Agonists of adrenergic and cholinergic receptors significantly influenced the in vitro activity of leukocytes from the rainbow trout, Salmo gairdneri. Agonists of beta-adrenergic receptors suppressed the in vitro antibody-secreting cell response and mitogen induced proliferation of leukocytes from the spleen, and the chemiluminescent response of pronephric leukocytes. The suppression induced by beta-receptor agonists could be blocked by beta-receptor antagonists. Agonists of alpha-adrenergic and cholinergic receptors enhanced both the in vitro antibody response and the chemiluminescent response. These effects were also blocked by the appropriate receptor antagonists. Alpha and cholinergic agonists had no effect on the mitogenic response. The alpha agonist-induced enhancement of the antibody response was found to be mediated by alpha-2 adrenergic receptors on rainbow trout splenic leukocytes.
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