|Salak-johnson, Janeen L.|
Submitted to: Physiology and Behavior
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/7/1996
Publication Date: N/A
Citation: N/A Interpretive Summary: Stress suppresses the immune system which promotes pathogenesis of infectious diseases and tumor development. Various stressors induce neuroendocrine alterations which suppress the immune system and, thus, decrease disease resistance. The link between the immune and neuroendocrine systems is poorly understood. An important physiological response to stress is activation of the hypothalamic-pituitary-adrenal axi Hypothalamic corticotropin releasing hormone (CRH) is the primary mediator of the stress response. CRH stimulates pituitary gland release of adrenocorticotropic hormone (ACTH) and peptides of the endogenous opioid peptide family. ACTH in turn stimulates adrenal gland secretion of cortisol. It has been generally accepted for a long time that stress- induced immunosuppression is mediated by cortisol. However, recent work showed that other mediators are involved: stress induced immunosuppression in normal as well as adrenalectomized rats. Researchers at Texas Tech University and the Richard B. Russell Agricultural Research Center showed that administration of CRH into the brain ventricular system produced dramatic behavioral changes and significant immunosuppression which was not mediated by the classically accepted mechanism of activation of the pituitary-adrenal axis. Such treatment appears to mimic acute rather than chronic stress response.
Technical Abstract: In Experiment 1, 50 ug of porcine corticotropin-releasing hormone (pCRH) or saline vehicle (V) was injected intracerebroventricularly (ICV). Plasma cortisol concentrations were higher after pCRH than after V. Generally, pCRH failed to alter NK cytotoxicity or lymphocyte proliferation in response to phytohemagluttin. Pigs injected with pCRH had lower neutrophil chemotaxis (CHTX) than controls. As blood cortisol concentration increased, neutrophil CHTX decreased. Pigs injected with pCRH had higher neutrophil numbers and neutrophil:lymphocyte ratios than controls. Percentage of lymphocytes was higher among control than treated pigs. Central pCRH increased overall activity and activity-related sequences (e.g., sit, walk and stand, walk), but reduced complex oral/nasal sequences (e.g., root, lick). In Experiment 2, pigs were injected ICV with 10 ug of cortisol or V. Cortisol failed to alter NK cytotoxicity, lymphocyte proliferation, CHTX, or leukocyte distribution and behavior. Thus, leukocyte distribution and specific neutrophil function were significantly modulated by stress-related hypothalamic-pituitary-adrenal axis hormones and complexity of behavioral sequences associated with increased activity was reduced. Oral/nasal stereotypies (as seen in confined sows) were not elevated by pCRH. CRH given ICV may better mimic acute rather than chronic stress.