Reciprocal Relationships Between the Neuroendocrine System and Lymphoid Cells
Westly, Hollie J.
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Permalink
https://hdl.handle.net/2142/70039
Description
Title
Reciprocal Relationships Between the Neuroendocrine System and Lymphoid Cells
Author(s)
Westly, Hollie J.
Issue Date
1986
Department of Study
Animal Sciences
Discipline
Animal Sciences
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Health Sciences, Immunology
Abstract
A wide variety of environmental and psychological stressors alter the susceptibility of animals to infectious and neoplastic diseases. However, physiologic mechanisms involved in these phenomena are not understood. Acute stressors activate both the hypothalamic-pituitary-adrenal axis and sympathomedullary system, which results in increased plasma concentrations of glucocorticoids and cathecholamines. Lymphoid cells possess receptors for both of these stress-related hormones, and activation of these receptors affects functional activities of lymphoid cells. In the present experiments, it is demonstrated that activation of porcine splenocytes with concanavalin A results in a two-fold increase in glucocorticoid and (beta)-adrenergic receptors with no change in the binding affinity of the receptor. Similarly, cortisol increases the number of (beta)-adrenoceptors on non-stimulated splenocytes. Cortisol prevents the concanavalin A-induced increase in glucocorticoid receptors while the (beta)-agonist, isoproterenol, prevents the mitogen-induced increase in (beta)-adrenoceptors. Both cortisol and isoproterenol increase the apparent dissociation constant of (beta)-adrenoceptors on concanavalin A-activated splenocytes, but this effect is time-related.
Bacterial and viral infections are associated with elevated levels of circulating plasma glucocorticoids. Both viral and bacterial agents can induce synthesis and secretion of adrenocorticotropin (ACTH) by lymphoid cells. ACTH, as well as six other peptide hormones from the pituitary gland, is derived from a 31 kd precursor protein known as pro-opiomelanocortin (POMC). However, it is not known if lymphocyte-derived ACTH is also derived from the POMC protein. To test the hypothesis that lymphocyte-derived ACTH is from the POMC protein, total cellular and poly(A)('+) cytoplasmic RNA were isolated from non-infected and Newcastle disease virus-infected (NDV) murine splenocytes. There was positive hybridization of both total cellular and poly(A)('+) cytoplasmic RNA isolated from NDV-infected splenocytes to a cDNA probe which contains the entire coding sequence for mouse POMC. Neither total cellular nor poly(A)('+) cytoplasmic RNA from non-infected splenocytes nor total cellular RNA isolated from mouse liver hybridized to the probe. Size of the mRNA from NDV-infected splenocytes was similar to mRNA from an ACTH-secreting mouse pituitary tumor cell line, AtT-20. These data provide evidence that virus-infected lymphoid cells synthesize the precursor protein for two "classical" pituitary hormones, ACTH and (beta)-endorphin, that are released during acute stress.
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