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      Role of the Brain in Interleukin-6 Modulation

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          Abstract

          High levels of interleukin 6 (IL-6) have been found in the brain tissue or cerebrospinal fluid (CSF) in several CNS disorders including Alzheimer’s disease, AIDS dementia complex, multiple sclerois, stroke, Parkinson’s disease, traumatic brain injuries, brain tumors and CNS infections. In these diseases, IL-6 is also found in blood showing that CNS conditions can elicit a peripheral immune response. A direct secretion of IL-6 from brain to blood has been shown to be a major mechanism by which the brain activates peripheral metabolic, endocrine and immune responses. However, this communication is not straightforward and other regulatory mechanisms are likely to be there. Several lines of evidence obtained in the laboratory have shown that the brain significantly modulates IL-6 production in the periphery. Evidence will be given that: (i) central inflammatory stimuli efficiently induce peripheral IL-6; (ii) central opioids are effective modulators of peripheral IL-6, and (iii) the sympathetic nervous system represents an inhibitory pathway to peripheral IL-6.

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          Most cited references 17

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          IL-6 and APPs: anti-inflammatory and immunosuppressive mediators.

          Acute inflammation is accompanied by changes in the concentrations of acute phase proteins (APPs). While much is known about the cytokines involved in the initiation of inflammation, less is known about the mediators involved in its resolution. Recent data suggest that interleukin 6 (IL-6) and IL-6-regulated APPs are anti-inflammatory and immuno-suppressive, and may negatively regulate the acute phase response.
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            Relationships between interleukin-6 activity, acute phase proteins, and function of the hypothalamic-pituitary-adrenal axis in severe depression.

            Recent studies from this laboratory have provided some evidence that major depression, in particular melancholia, may be accompanied by an immune response. The present study was designed to investigate whether severe depression is characterized by increased interleukin-6 (Il-6) activity and whether Il-6 production is related to altered levels of acute phase reactants and to abnormal function of the hypothalamic-pituitary-adrenal (HPA) axis. Measurements were made in 8 healthy control subjects and 24 depressed inpatients of Il-6 production in culture supernatants of mitogen-stimulated peripheral leukocytes and plasma levels of haptoglobin (Hp), transferrin (Tf), and postdexamethasone cortisol. Il-6 activity was significantly higher in melancholic subjects than in healthy control subjects and in patients with minor depression or nonmelancholic major depression. Il-6 production was significantly correlated with Hp (positively) and Tf (negatively) plasma levels. There were significant and positive correlations between Il-6 activity and postdexamethasone cortisol values. The findings may suggest that increased Il-6 activity in severe depression is related to hypotransferrinemia, hyperhaptoglobinemia, and hyperactivity of the HPA axis.
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              Proinflammatory cytokines in serum of patients with acute cerebral ischemia: kinetics of secretion and relation to the extent of brain damage and outcome of disease.

              The release of the proinflammatory cytokines IL-1 beta, IL-6, TNF-alpha and soluble TNF-receptors p55 and p75 in peripheral blood was serially determined in 19 patients with acute cerebral ischemia. Only patients admitted within 4 h following onset of symptoms were studied. In contrast to serum levels of IL-1 beta, TNF-alpha and TNF-receptors, which did not exhibit a significant response, IL-6 showed a significant increase of serum levels already within the first hours following onset of disease and reached a plateau at 10 h until day 3 and returned to baseline by day 7. The increase of levels of this cytokine was significantly (P < 0.05) correlated with increasing volumes of brain lesion and was also significantly (P < 0.005) associated with poor functional and neurological outcome. The increase of levels of IL-6 despite a considerable dilution in peripheral blood shown in this preliminary study suggests an early inflammatory response in ischemic brain lesion.
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                Author and article information

                Journal
                NIM
                Neuroimmunomodulation
                10.1159/issn.1021-7401
                Neuroimmunomodulation
                S. Karger AG
                978-3-8055-6766-4
                978-3-318-00353-6
                1021-7401
                1423-0216
                1998
                August 1998
                04 September 1998
                : 5
                : 3-4
                : 214-219
                Affiliations
                Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy
                Article
                26339 Neuroimmunomodulation 1998;5:214–219
                10.1159/000026339
                9730688
                © 1998 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 1, Tables: 1, References: 72, Pages: 6
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