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      Exhaustive Exercise Reduces Tumor Necrosis Factor-α Production in Response to Lipopolysaccharide in Mice

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          Abstract

          Objective: Stressful exercise reduces the plasma pro-inflammatory cytokine concentration in response to lipopolysaccharide (LPS). The aim of this study was to clarify the mechanism of exhaustive exercise-induced suppression of the plasma tumor necrosis factor (TNF)-α concentration in response to LPS. Methods: Male C3H/HeN mice (n = 66) were randomized to treadmill running to exhaustion (Ex) or a sedentary (Non-Ex) condition. Monocytes and splenic macrophages were collected from some animals, and other animals were injected with LPS (1 mg/kg) immediately after the exercise. The liver, lung and spleen tissues in the mice were removed 30 min after the LPS injection for determination of TNF-α mRNA expression. Blood and tissue samples were collected for determination of TNF-α and TNF receptors (TNFR) 1 h after the LPS injection. Results: Although there was a significant suppression in LPS-induced plasma TNF-α in the Ex mice when compared to the Non-Ex mice (p < 0.01), soluble TNFR in plasma was not affected by the exercise. There was no change in cell-surface expression of Toll-like receptor 4 (TLR4) and in LPS-induced TNF-α mRNA expression and TNFR content in tissues between the Ex and Non-Ex groups. Interestingly, TNF-α contents in the liver, lung and spleen of the Ex mice were significantly lower than those of the Non-Ex group (p < 0.01, p < 0.01 and p < 0.05, respectively). Conclusion: These data suggest that exhaustive exercise-induced suppression of the plasma TNF-α concentration despite LPS stimulation might depend on translation of TNF-α in tissues.

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          The effects of moderate exercise training on natural killer cells and acute upper respiratory tract infections.

          Meghan A. Balk, K Arabatzis, D Nieman … (1990)
          A randomly controlled 15-wk exercise training (ET) study (five 45-min sessions/wk, brisk walking at 60% heart rate reserve) with a group of 36 mildly obese, sedentary women was conducted to investigate the relationship between improvement in cardiorespiratory fitness, changes in natural killer (NK) cell number and activity, and acute upper respiratory tract infection (URI) symptomatology. The study was conducted using a 2 (exercise and nonexercise groups) x 3 (baseline, 6-, and 15-wk testing sessions) factorial design, with data analyzed using repeated measures ANOVA. No significant change in NK cell number occurred as a result of ET as measured by the CD16 and Leu-19 monoclonal antibodies. ET did have a significant effect on NK cell activity (E:T 50:1) especially during the initial 6-wk period [F(2.68) = 12.34, p less than 0.001]. Using data from daily logs kept by each subject, the exercise group was found to have significantly fewer URI symptom days/incident than the nonexercise group (3.6 +/- 0.7 vs 7.0 +/- 1.4 days, respectively, p = 0.049). Improvement in cardiorespiratory fitness was correlated significantly with a reduction in URI symptom days/incident (r = 0.37, p = 0.025) and a change in NK cell activity from baseline to six but not 15 wks (r = 0.35, p = 0.036). In summary, moderate ET is associated with elevated NK cell activity after six but not 15 weeks, and reduced URI symptomatology in comparison to a randomized, sedentary control group.
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            NK cell response to physical activity: possible mechanisms of action.

            H Ullum, Dan B Pedersen (1994)
            Natural killer (NK) cells are highly influenced by physical exercise. The possible important mechanisms behind exercise-induced changes in NK cell function are cytokines, hyperthermia, and stress hormones, including catecholamines, growth hormone, cortisol, and beta-endorphins. Infusion studies mimicking stress hormone levels in blood during exercise indicate that increased plasma-adrenaline accounts for at least part of the exercise-induced modulation of NK cell function. During moderate as well as severe acute exercise, the NK cell activity is enhanced, but severe exercise is followed by immunodepression, at least in part caused by prostaglandins. Elite athletes have at rest elevated NK cell activity. However, due to frequent severe exercise the NK cell function is often temporarily severely depressed. It is suggested that during the time of immunodepression microorganisms, especially virus, invade the host, whereby infections can be established. However, in those who perform regular moderate exercise the immune system will often be temporarily enhanced and this will protect these from infections.
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              The physiological regulation of toll-like receptor expression and function in humans.

              Daniel F. Wallace, Ian Drysdale, Irum Khan … (2005)
              Eleven mammalian toll-like receptors (TLRs 1-11) have been identified to date and are known to play a crucial role in the regulation of immune responses; however, the factors that regulate TLR expression and function in vivo are poorly understood. Therefore, in the present study, we investigated the physiological regulation of TLR expression and function in humans. To examine the influence of diurnal rhythmicity on TLR expression and function, peripheral venous blood samples were collected from healthy volunteers (n = 8) at time points coinciding with the peak and nadir in the endogenous circulating cortisol concentration. While no diurnal rhythmicity in the expression of TLRs 1, 2, 4 or 9 was observed, the upregulation of costimulatory (CD80 and CD86) and antigen-presenting (MHC class II) molecules on CD14(+) monocytes following activation with specific TLR ligands was greater (P < 0.05) in samples obtained in the evening compared with the morning. To examine the influence of physical stress on TLR expression and function, peripheral venous blood samples were collected from healthy volunteers (n = 11) at rest and following 1.5 h of strenuous exercise in the heat (34 degrees C). Strenuous exercise resulted in a decrease (P < 0.005) in the expression of TLRs 1, 2 and 4 on CD14(+) monocytes. Furthermore, the upregulation of CD80, CD86, MHC class II and interleukin-6 by CD14(+) monocytes following activation with specific TLR ligands was decreased (P < 0.05) in samples obtained following exercise compared with at rest. These results demonstrate that TLR function is subject to modulation under physiological conditions in vivo and provide evidence for the role of immunomodulatory hormones in the regulation of TLR function.
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                Author and article information

                Journal
                Journal ID (publisher-id): NIM
                Journal ID (nlm-ta): Neuroimmunomodulation
                Journal ID (doi): 10.1159/issn.1021-7401
                Title: Neuroimmunomodulation
                Publisher: S. Karger AG
                ISSN (Print): 1021-7401
                ISSN (Electronic): 1423-0216
                Publication date Subscription-year: 2010
                Publication date (Print): March 2010
                Publication date (Electronic): 05 March 2010
                Volume: 17
                Issue: 4
                Pages: 279-286
                Affiliations
                aDepartment of Health and Sports Science, Kawasaki University of Medical Welfare, Kurashiki, bDepartment of Cytology and Histology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, cConsolidated Research Institute for Advanced Science and Medical Care, Waseda University, Tokyo, dExercise Physiology Laboratory, Wayo Women’s University, Ichikawa, and eDivision in Health Science, Kawasaki University of Medical Welfare, Kurashiki, Japan
                Author notes
                *Hiromi Yano, PhD, Department of Health and Sports Science, Kawasaki University of Medical Welfare, 288 Matsushima, Kurashiki, OK 701-0193 (Japan), Tel. +81 86 462 1111, Fax +81 86 464 1199, E-Mail yanohiro@mw.kawasaki-m.ac.jp
                Article
                Publisher ID: 290044 Other ID: Neuroimmunomodulation 2010;17:279–286
                DOI: 10.1159/000290044
                PubMed ID: 20203534
                SO-VID: a8bfade0-a9ed-4f75-b550-3aaced2e5c56
                Copyright © © 2010 S. Karger AG, Basel
                License:

                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.

                History
                Date received : 14 April 2009
                Date accepted : 21 August 2009
                Page count
                Figures: 6, References: 34, Pages: 8
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Endocrinology & Diabetes,Neurology,Nutrition & Dietetics,Sexual medicine,Internal medicine,Pharmacology & Pharmaceutical medicine
                Keywords: Immune suppression,Toll-like receptor 4,Lipopolysaccharide,Tumor necrosis factor-α,TNF receptors
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes, Neurology, Nutrition & Dietetics, Sexual medicine, Internal medicine, Pharmacology & Pharmaceutical medicine
                Keywords: Immune suppression, Toll-like receptor 4, Lipopolysaccharide, Tumor necrosis factor-α, TNF receptors

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