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Effect of cholinergic agonists and antagonists on experimental allergic encepalomyelitis
STAPHYLOCOCCAL ENTEROTOXIN MODULATES CLINICAL MANIFESTATION OF AUTOIMMUNE ENCEPHALOMYELITIS Yoh Matsumoto, Katsutoshi O h m o r i and Michio Fujiwara, Department of Immunology, Niigata University School of Medicine, Niigata 951, Japan The development or suppression of autoimmune disease is heavily influenced by a preceding or coexisting episode of infection. There are several explanations for this relationship. First, due to "molecular mimicry" between components of infectious agents and autoantigens, T ly~phocytes generated to infectious agents attack self antigens, resultin~ in the development of autoimmune diseases. Second, some toxins released by bacteria stimulate prolif:ration of a certain type of T cells, after which autoimmune diseases develop. Third, up-regulation of heat shock protein(I-ISP) in response to infection stimulates HSP-reactive 3' 5+ T cells to produce IL-2. IL-2, in turn, activates autoreactive a [3+ T cells which has been at a tolerant .~tate. Using a cortain type of staphylococcal enterotoxin, we have confirmed that the mechanism raised as the second possibility is, in fact, generated in the development of experimental autoimmune encephalomyelitis(EAE). Administration of the toxin prior to, but not after, antigen challenge, protected Lewis rats from the development of EAE. Unexpectedly, however, responses of lymph node cells from the protected rats to SED and myelin basic protein were not suppressed or deleted. These findings suggested that suppressor cells may play an important role in this type of protection.
EFFECT OF CHOLINERGIC AGONISTS AND ANTAGONISTS ON EXPERIMENTAL ALLERGIC ENCEPALOMYELITIS 'Bane Anlar) M a r k A. Jensen) Anthony T. Reder) and Barry G.W. Amason, The University of Chicago, Chicago IL USA Cholinergic agonists increase lymphocyte cytotoxicity, motility, rosette formation, antibody production and proliferation in vitro. Inanune organs are innervated and immune functions are affected by the autonomic nervous system. Sympathetic ablation increases the severity of experimental allergic encephalomyelitis (EAE) in rats. Local parasympathectomy, however, decreases plaque-forming cell responses in submandibular lymph nodes. We examined the effect of carbachol, a cholinergic agonist, and scopoiamine, in antagonist, on EAE in Lewis rats. Disease was actively induced by injection of 0.2 ml adjuvant (25% w]v of guinea pig spinal cord in IFA supplemented with 3 m~ml of Mycol~ctenuta tuberculosis') into each hind footpad. Carbachol (250)~glkg., b.i.d.), scopolamine (20 •mglkg., b.i.d.), or saline were injected subcutaneously starting with the day of immunization. Disease onset was significantly delayed (p< 0.05), clinical scores lower (!)<0.05), and duration of disease shorter (p<0.01) in the scopolamine-injected rats compared to the saline group. The carbacliol group did not differ significantly from the control rats. These data suggest a protective role for cholinergic antagonists in EAE.
EFFECT OF CHOLINERGIC AGONISTS AND ANTAGONISTS ON EXPERIMENTAL ALLERGIC ENCEPALOMYELITIS 'Bane Anlar) M a r k A. Jensen) Anthony T. Reder) and Barry G.W. Amason, The University of Chicago, Chicago IL USA Cholinergic agonists increase lymphocyte cytotoxicity, motility, rosette formation, antibody production and proliferation in vitro. Inanune organs are innervated and immune functions are affected by the autonomic nervous system. Sympathetic ablation increases the severity of experimental allergic encephalomyelitis (EAE) in rats. Local parasympathectomy, however, decreases plaque-forming cell responses in submandibular lymph nodes. We examined the effect of carbachol, a cholinergic agonist, and scopoiamine, in antagonist, on EAE in Lewis rats. Disease was actively induced by injection of 0.2 ml adjuvant (25% w]v of guinea pig spinal cord in IFA supplemented with 3 m~ml of Mycol~ctenuta tuberculosis') into each hind footpad. Carbachol (250)~glkg., b.i.d.), scopolamine (20 •mglkg., b.i.d.), or saline were injected subcutaneously starting with the day of immunization. Disease onset was significantly delayed (p< 0.05), clinical scores lower (!)<0.05), and duration of disease shorter (p<0.01) in the scopolamine-injected rats compared to the saline group. The carbacliol group did not differ significantly from the control rats. These data suggest a protective role for cholinergic antagonists in EAE.