We have shown that the sympathetic nervous system (SNS) modulates immune responses. We have presented data showing that ablation of the SNS augments immune responses, changes the proportions of lymphocytes subsets, increases the number of beta adrenergic receptors on the lymphocyte surface, changes the function and number of natural killer cells and augments the severity of 2 experimentally autoimmune diseases: Experimental Allergic Encephalomyelitis (EAE) and experimental autoimmune myasthenia gravis (EAMG). We will now study the influence of the SNS on macrophage function. Macrophages play an essential part in the immune response and release a number of biologically active molecules involved in host defense, inflammation and protection against malignancy. Some macrophage-secreted factors may also play a major role in the pathology of chronic inflammatory disease when the macrophage response to normally occurring stimuli is exaggerated. We will study macrophage function in sympathectomized animals by measuring secretion of Interleukin-1, Tumor Necrosis Factor/Cachectin and expression of MHC class II antigens on the macrophage surface. We will continue to study EAE in SNS-ablated and control animals with emphases on the roles of macrophages, T cell and antibodies against myelin basic protein in this disease and of the influence of SNS ablation on these responses. In this way we hope to determine the mechanisms responsible for the augmentation of EAE in animals with an ablated SNS. We will also study the influence of beta adrenergic agonists and antagonists on macrophage function seeking to reverse the abnormalities that follow SNS ablation. We believe that an understanding of how the SNS regulates the immune system, and in particular macrophage function, may have an impact on prevention and treatment of immune-mediated diseases.

National Institute of Health (NIH)
National Institute of Neurological Disorders and Stroke (NINDS)
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Neurology C Study Section (NEUC)
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University of Chicago
Schools of Medicine
United States
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Chelmicka-Schorr, E; Wollmann, R L; Kwasniewski, M N et al. (1993) The beta 2-adrenergic agonist terbutaline suppresses acute passive transfer experimental autoimmune myasthenia gravis (EAMG). Int J Immunopharmacol 15:19-24
Chelmicka-Schorr, E; Kwasniewski, M N; Czlonkowska, A (1992) Sympathetic nervous system and macrophage function. Ann N Y Acad Sci 650:40-5
Chelmicka-Schorr, E; Kwasniewski, M N; Wollmann, R L (1992) Sympathectomy augments adoptively transferred experimental allergic encephalomyelitis. J Neuroimmunol 37:99-103
Chelmicka-Schorr, E; Kwasniewski, M N; Czlonkowska, A (1992) Sympathetic nervous system modulates macrophage function. Int J Immunopharmacol 14:841-6
Chelmicka-Schorr, E; Arnason, B G (1990) Nervous system-immune system interactions. Res Publ Assoc Res Nerv Ment Dis 68:67-90
Chelmicka-Schorr, E; Checinski, M E; Arnason, B G (1990) Sympathetic nervous system and PC12 pheochromocytoma-derived factors suppress stimulation of lymphocytes. Brain Behav Immun 4:23-9
Chelmicka-Schorr, E; Kwasniewski, M N; Thomas, B E et al. (1989) The beta-adrenergic agonist isoproterenol suppresses experimental allergic encephalomyelitis in Lewis rats. J Neuroimmunol 25:203-7
Chelmicka-Schorr, E; Checinski, M E; Arnason, B G (1989) PC12 pheochromocytoma and sympathetic nervous system derived trophic factors augment growth of neuroblastoma. Eur J Cancer Clin Oncol 25:1057-9
Reder, A; Checinski, M; Chelmicka-Schorr, E (1989) The effect of chemical sympathectomy on natural killer cells in mice. Brain Behav Immun 3:110-8
Chelmicka-Schorr, E; Checinski, M E (1989) Sympathetic nervous system derived trophic factor augments growth of human neuroblastoma in vitro. Eur J Cancer Clin Oncol 25:393-4

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