+1 Recommend
1 collections
      • Record: found
      • Abstract: found
      • Article: found

      Prostaglandin E 2 and Bacterial Lipopolysaccharide Stimulate Bioactive Interleukin-1 Release from Rat Hypothalamic Explants

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          While interleukin-1 (IL-1) is intimately involved in locally modulating the acute inflammatory response, it is also able to influence processes at remote sites, i.e., in an endocrine manner. While there is as yet little evidence that IL-1 can cross the blood-brain barrier, many effects such as fever, increased slow-wave sleep, anorexia and the modulation of neuroendocrine function suggest an action of circulating IL-1 at regulatory sites within the hypothalamus. However, there is accumulating evidence for IL-1 originating within the central nervous system (CNS), and it is currently unclear as to whether the neurally mediated manifestations of the acute inflammatory response are due to activation of central or peripheral (circulating) IL-1. In this study we have characterized the release of IL-1 from rat hypothalamic explants, and we have investigated the effects of putative modulators of IL-1 release, lipopolysaccharide (LPS) and the prostaglandins E<sub>2</sub> (PGE<sub>2</sub>) and F<sub>2α</sub> (PGF<sub>2α</sub>). After 1 h of incubation, IL-1-like activity in hypothalamic supernatants ranged between 175 and 2,304 munits/mg of protein; this was substantially inhibited by the addition to the bioassay system of antibodies (1:200) against IL-1α, but not against IL-1β. LPS and PGE<sub>2</sub> significantly stimulated IL-1 release at 100 and 1 ng/ml respectively, whereas PGF<sub>2α</sub> had no effect in the range of doses tested. It is therefore concluded that the control of hypothalamic IL-1 release may be investigated by means of acute rat hypothalamic explants. Furthermore, both LPS and PGE<sub>2</sub> can stimulate IL-1 release in this model, although no clear dose-response relationship could be discerned. Taking into account previous studies which have shown that IL-1 may specifically stimulate the release of hypothalamic PGE<sub>2</sub>, these data suggest that (1) PGE<sub>2</sub> may mediate communication between circulating and CNS-derived IL-1, and (2) the effects of LPS on neuroendocrine function may occur, at least in part, independent of circulating IL-1.

          Related collections

          Author and article information

          S. Karger AG
          08 April 2008
          : 57
          : 2
          : 257-261
          aDepartment of Pharmacology, Catholic University Medical School, Rome, bIRIS Research Center, Siena, Italy; cDepartment of Endocrinology, St. Bartholomew’s Hospital, London, UK
          126367 Neuroendocrinology 1993;57:257–261
          © 1992 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
          Pages: 5
          Original Paper


          Comment on this article