Journal Mobile Options
Table of Contents
Vol. 118, No. 2-4, 1999
Issue release date: February–April 1999
Int Arch Allergy Immunol 1999;118:375–379
(DOI:10.1159/000024141)

Regulation of Proinflammatory Cytokines in Seasonal Allergic Rhinitis

Bachert C. · van Kempen M. · van Cauwenberge P.
ENT Department, University Hospital Ghent, Belgium

Individual Users: Register with Karger Login Information

Please create your User ID & Password





Contact Information











I have read the Karger Terms and Conditions and agree.

To view the fulltext, please log in

To view the pdf, please log in

Abstract

Background: Mediators and cytokines have been demonstrated to be released due to nasal allergen exposure in sensitized subjects, but little is known about the release of cytokines and their antagonists under natural conditions. Methods: Mediators – histamine, eosinophilic cationic protein (ECP), leukotrienes (LT) C4/ D4/E4 – and cytokines – interleukin (IL)–1β, IL–8, IL–1 receptor antagonist (ra) – were measured in nasal secretions throughout the grass pollen season (6 visits) and for 6 weeks thereafter (3 visits) in patients with seasonal allergic rhinitis (n = 13) and compared to controls (n = 12). A second study was performed comparing nasal secretions of 13 subjects allergic to house dust mite to 8 controls. Results: Compared to controls, leukotrienes and ECP were significantly elevated at nearly all time points in and postseason in the allergic group. Whereas IL–1β was significantly elevated throughout the study period, IL–1ra was significantly decreased from visit 1 to 3. IL–8 showed no increase compared to controls. Data from subjects with perennial allergic rhinitis supported these findings and additionally demonstrated decreased concentrations of IL–8 and myeloperoxidase in secretions compared to controls. Conclusion: Allergic rhinitis represents a persistent inflammation in terms of an activation of eosinophils and constant upregulation of the proinflammatory cytokine IL–1β in the pollen season and thereafter. We additionally could demonstrate a dysfunction of the anti–inflammatory capacity, i.e. IL–1ra, a naturally occurring antagonist. Persistent inflammation may furthermore lead to the dysregulation of local cellular immunity by reducing the number and activity of neutrophils on the mucosal surface.



Copyright / Drug Dosage

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 or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center.
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 goverment 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.

References

  1. Naclerio RM, Proud D,Togias AG, Adkinson NF, Meyers DA, Kagey–Sobotka A, Plaut M, Norman PS, Lichtenstein LM: Inflammatory mediators in late antigen–induced rhinitis. N Engl J Med 1985;313:65–70.
  2. Wang D, Clement P, Smitz J, De Waele M, Derde MP: Correlations between complaints, inflammatory cells and mediator concentrations in nasal secretions after nasal allergen challenge and during natural allergen exposure. Int Arch Allergy Immunol 1995;106: 278–285.
  3. Bousquet J, Vignola AM, Campbell AM, Michel FB: Pathophysiology of allergic rhinitis. Int Arch Allergy Immunol 1996;110:207– 218.

    External Resources

  4. Ciprandi G, Buscaglia S, Pesce G: Minimal persistent inflammation is present at mucosal level in patients with asymptomatic rhinitis and mite allergy. J Allergy Clin Immunol 1995;96:971–979.
  5. Gosset P, Malaquin F, Delneste Y: Interleukin–6 and interleukin–1 production is associated with antigen–induced late nasal response. J Allergy Clin Immunol 1993;92:878–890.
  6. Sim TC, Grant JA, Hilsmeier KA, Fukuda Y, Alam R: Proinflammatory cytokines in nasal secretions after antigen challenge. Am J Respir Crit Care Med 1994;149:339–344.
  7. Bachert C, Wagenmann M, Holtappels G: Cytokines and adhesion molecules in allergic rhinitis. Am J Rhinol 1998;12:3–8.
  8. Bachert C, Wagenmann M, Hauser U: Proinflammatory cytokines: Measurement in nasal secretions, induction of adhesion receptor expression. Int Arch Allergy Immunol 1995;107: 106–108.


Pay-per-View Options
Direct payment This item at the regular price: USD 38.00
Payment from account With a Karger Pay-per-View account (down payment USD 150) you profit from a special rate for this and other single items.
This item at the discounted price: USD 26.50