Effect of Interferon-γ Treatment on 24-Hour Variations in Plasma ACTH, Growth Hormone, Prolactin, Luteinizing Hormone and Follicle-Stimulating Hormone of Male Rats

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Abstract

Objective: Interferon-γ (IFN-γ) is a cytokine produced by T helper cells on antigenic challenge that may affect the release of several pituitary hormones. However, in vitro or in vivo studies have yielded disparate results with stimulatory, inhibitory or absent effects of IFN on pituitary hormone release. One of the reasons for these discrepancies could be that hormone changes were commonly assessed at a single time point in the day-night cycle. In this study we measured the circadian pattern of plasma ACTH, growth hormone (GH), prolactin, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) at 6 different time points within a 24-hour cycle in adult male Wistar rats. Methods: Groups of 6–8 rats kept under light from 08:00 to 20:00 h daily received 5 daily injections intraperitoneally of human IFN-γ (10<sup>5</sup> IU/kg body weight) or saline at 08:30 h. Plasma ACTH, GH, prolactin, LH and FSH levels were measured by a homologous specific double antibody RIA. Results: A factorial ANOVA for main effects indicated a significant 43% increase of circulating prolactin in IFN-γ-treated rats. Time of day changes were significant for the five hormones examined and these diurnal variations became altered by IFN-γ administration, with a phase advance of ACTH peak, a suppression of the rest phase peak of GH, the appearance of a second peak of prolactin at an early phase of daily photoperiod, and the blunting of the 24-hour variations of plasma FSH. Conclusion: The data point out an effect of IFN-γ on the mechanisms responsible for the circadian organization of pituitary hormone release.

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Cytokine-induced sickness behavior: mechanisms and implications.

Robert Dantzer (2001)

Sickness behavior refers to a coordinated set of behavioral changes that develop in sick individuals during the course of an infection. At the molecular level, these changes are due to the brain effects of proinflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor alpha (TNFalpha). Peripherally released cytokines act on the brain via a fast transmission pathway involving primary afferent nerves innervating the bodily site of inflammation and a slow transmission pathway involving cytokines originating from the choroid plexus and circumventricular organs and diffusing into the brain parenchyma by volume transmission. At the behavioral level, sickness behavior appears to be the expression of a central motivational state that reorganizes the organism priorities to cope with infectious pathogens. There is evidence that the sickness motivational state can interact with other motivational states and respond to nonimmune stimuli probably by way of sensitization and/or classical conditioning. However, the mechanisms that are involved in plasticity of the sickness motivational state are not yet understood.

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The concept of sickness behavior: a brief chronological account of four key discoveries.

R.W. Johnson (2002)

Neurons do not have receptors to detect bacteria or viruses, yet the presence of these microorganisms can cause a sickness behavior syndrome that includes, e.g., fever, anorexia, and lethargy. Because the immune system has receptors capable of detecting these non-cognitive stimuli, how the immune system transmits a message to the brain has been studied to understand why behavior is altered in sick animals. The focus has been on several cytokines secreted by leukocytes; these include interleukin (IL)-1beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha). These cytokines are secreted by activated mononuclear phagocytic cells, and numerous studies show that both peripheral and central injection of IL-1beta, IL-6, and TNF-alpha induce sickness behavior. Moreover, these cytokines and their receptors are present in the brain and inhibiting the secretion of cytokines or blocking their receptors in the brain blocks or abrogate the behavioral responses induced by inflammatory stimuli. Because the sickness behavior syndrome modulates the immune system and enhances recovery, the interplay between the immune system and central nervous system is an essential part of the overall host defense against pathogenic microorganisms. The purpose of this brief paper is to provide a chronological description of four critical advances that have led to the current understanding of how the immune system communicates with the brain to induce sickness behavior. Results from several key studies will be discussed, which showed that: (1) sickness behavior is a motivational state; (2) sickness behavior is a well-organized adaptive response to infection; (3) cytokines produced by activated leukocytes induce sickness behavior; and (4) cytokines transmit messages from the periphery to the brain using humoral and neural pathways.

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Changing the dosing schedule minimizes the disruptive effects of interferon on clock function.

S Higuchi, H Aramaki, S Koyanagi … (2001)

The effectiveness and toxicity of many drugs vary depending on the relationship between the dosing schedule and the 24-hour rhythms of biochemical, physiological and behavioral processes. In addition, several drugs can cause alterations to the 24-hour rhythms leading to illness and altered homeostatic regulation. However, the mechanisms of this drug-based disruption of circadian 'clock' genes remain unclear. Here, we show the disruptive effect of interferon-alpha on the rhythm of locomotor activity, body temperature and clock-gene mRNA expression in the periphery and suprachiasmatic nuclei, a primary circadian pacemaker. The rhythmicity of clock genes and the photic induction of the Per gene in suprachiasmatic nuclei were disturbed by the repetitive administration of interferon-alpha. Moreover, alteration of clock function, a new concept of adverse effects, can be overcome by optimizing the dosing schedule to minimize adverse drug effects.

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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: 2005

Publication date (Print): May 2005

Publication date (Electronic): 17 May 2005

Volume: 12

Issue: 3

Pages: 146-151

Affiliations

^aDepartamento de Bioquímica y Biología Molecular III y ^bDepartamento de Biología Celular, Facultad de Medicina, Universidad Complutense, Madrid, España; ^cDepartamento de Fisiología, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina

Article

Publisher ID: 84846 Other ID: Neuroimmunomodulation 2005;12:146–151

DOI: 10.1159/000084846

PubMed ID: 15905622

SO-VID: 96806c4c-6964-4d5c-bccd-0f988a9dff05

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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 : 11 February 2004

Date accepted : 11 August 2004

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Figures: 2, References: 43, Pages: 6

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Effect of Interferon-γ Treatment on 24-Hour Variations in Plasma ACTH, Growth Hormone, Prolactin, Luteinizing Hormone and Follicle-Stimulating Hormone of Male Rats

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Karger: Endocrinology

Most cited references 28

Cytokine-induced sickness behavior: mechanisms and implications.

The concept of sickness behavior: a brief chronological account of four key discoveries.

Changing the dosing schedule minimizes the disruptive effects of interferon on clock function.

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