The University of Southampton
University of Southampton Institutional Repository

Lower airways inflammation in allergic rhinitics: a comparison with asthmatics and normal controls

Lower airways inflammation in allergic rhinitics: a comparison with asthmatics and normal controls
Lower airways inflammation in allergic rhinitics: a comparison with asthmatics and normal controls
Background: allergic rhinitis (AR) and asthma represent a continuum of atopic disease. AR is believed to pre-dispose an individual to asthma. Compared with asthmatics and normal controls, the inflammatory response in the lower airways of rhinitics is not fully elucidated. To test the hypothesis that the inflammatory response in the airways of subjects with AR is at a level intermediate between that in normal controls and asthmatics, we have characterized bronchial inflammation and cytokine mRNA levels in non-asthmatic allergic rhinitics and compared it with subjects with allergic asthma and with normal controls.

Methods: endobronchial mucosal biopsies were obtained at bronchoscopy from 14 allergic rhinitics, 16 asthmatics and 21 normal controls. Biopsies were embedded into glycol methacrylate resin for immunohistochemical analysis of cellular inflammation and snap frozen for semi-quantitative PCR analysis of cytokine mRNA levels.

Results: airway inflammation in rhinitic subjects was characterized by an increase in submucosal eosinophils, mast cells and the mRNA expression of TNF-?, at an intermediate level between healthy and asthmatics. In addition, CD3+ and CD8+ lymphocytes in the epithelium, the endothelial expression of vascular adhesion molecule-1 and IL-1? mRNA were higher in the allergic rhinitics compared with both normal controls and asthmatics, whereas growth-related oncogene ?-mRNA was decreased in AR compared with both healthy and asthmatics. Airway inflammation in the asthmatic group was characterized by higher numbers of eosinophils and mast cells, together with an increase in TNF-?-mRNA compared with both healthy and rhinitics. IFN-? mRNA was the highest in normal controls and lowest in the asthmatics.

Conclusions: tn individuals with AR the present data suggest an intermediate state of airway inflammation between that observed in normal individuals and subjects with clinical asthma. It is also indicated that IFN-? production by CD8+ T lymphocytes could be protective against the development of airway hyperresponsiveness. Further work is needed to evaluate this hypothesis
0954-7894
688-695
Brown, J.L.
2242e179-ae74-4127-9625-b821c49a7a0b
Behndig, A.F.
931c99ae-ee43-4211-93fd-e033286f4182
Sekerel, B.E.
a0f7be0b-3464-42dd-a7e4-0d324a65d0d6
Pourazar, J.
8cf3c9a6-c253-4602-86a4-331209a703a7
Blomberg, A.
11132832-def7-4683-8a08-51dbe11581f0
Kelly, F.J.
0662f749-2cc5-465a-a4aa-2a6ff64146ac
Sandström, T.
d3d026b6-08f7-4c4b-acc4-9c621390af69
Frew, A.J.
c00e9630-a5f0-44b3-add0-44b68836bbcb
Wilson, S.J.
21c6875d-6870-441b-ae7a-603562a646b8
Brown, J.L.
2242e179-ae74-4127-9625-b821c49a7a0b
Behndig, A.F.
931c99ae-ee43-4211-93fd-e033286f4182
Sekerel, B.E.
a0f7be0b-3464-42dd-a7e4-0d324a65d0d6
Pourazar, J.
8cf3c9a6-c253-4602-86a4-331209a703a7
Blomberg, A.
11132832-def7-4683-8a08-51dbe11581f0
Kelly, F.J.
0662f749-2cc5-465a-a4aa-2a6ff64146ac
Sandström, T.
d3d026b6-08f7-4c4b-acc4-9c621390af69
Frew, A.J.
c00e9630-a5f0-44b3-add0-44b68836bbcb
Wilson, S.J.
21c6875d-6870-441b-ae7a-603562a646b8

Brown, J.L., Behndig, A.F., Sekerel, B.E., Pourazar, J., Blomberg, A., Kelly, F.J., Sandström, T., Frew, A.J. and Wilson, S.J. (2007) Lower airways inflammation in allergic rhinitics: a comparison with asthmatics and normal controls. Clinical & Experimental Allergy, 37 (5), 688-695. (doi:10.1111/j.1365-2222.2007.02695.x). (PMID:17456216)

Record type: Article

Abstract

Background: allergic rhinitis (AR) and asthma represent a continuum of atopic disease. AR is believed to pre-dispose an individual to asthma. Compared with asthmatics and normal controls, the inflammatory response in the lower airways of rhinitics is not fully elucidated. To test the hypothesis that the inflammatory response in the airways of subjects with AR is at a level intermediate between that in normal controls and asthmatics, we have characterized bronchial inflammation and cytokine mRNA levels in non-asthmatic allergic rhinitics and compared it with subjects with allergic asthma and with normal controls.

Methods: endobronchial mucosal biopsies were obtained at bronchoscopy from 14 allergic rhinitics, 16 asthmatics and 21 normal controls. Biopsies were embedded into glycol methacrylate resin for immunohistochemical analysis of cellular inflammation and snap frozen for semi-quantitative PCR analysis of cytokine mRNA levels.

Results: airway inflammation in rhinitic subjects was characterized by an increase in submucosal eosinophils, mast cells and the mRNA expression of TNF-?, at an intermediate level between healthy and asthmatics. In addition, CD3+ and CD8+ lymphocytes in the epithelium, the endothelial expression of vascular adhesion molecule-1 and IL-1? mRNA were higher in the allergic rhinitics compared with both normal controls and asthmatics, whereas growth-related oncogene ?-mRNA was decreased in AR compared with both healthy and asthmatics. Airway inflammation in the asthmatic group was characterized by higher numbers of eosinophils and mast cells, together with an increase in TNF-?-mRNA compared with both healthy and rhinitics. IFN-? mRNA was the highest in normal controls and lowest in the asthmatics.

Conclusions: tn individuals with AR the present data suggest an intermediate state of airway inflammation between that observed in normal individuals and subjects with clinical asthma. It is also indicated that IFN-? production by CD8+ T lymphocytes could be protective against the development of airway hyperresponsiveness. Further work is needed to evaluate this hypothesis

Full text not available from this repository.

More information

e-pub ahead of print date: 20 April 2007
Published date: May 2007

Identifiers

Local EPrints ID: 190901
URI: https://eprints.soton.ac.uk/id/eprint/190901
ISSN: 0954-7894
PURE UUID: 58b07325-5a43-4da0-aa3d-c844e2a3b02e

Catalogue record

Date deposited: 16 Jun 2011 10:37
Last modified: 28 Jun 2018 16:31

Export record

Altmetrics

Contributors

Author: J.L. Brown
Author: A.F. Behndig
Author: B.E. Sekerel
Author: J. Pourazar
Author: A. Blomberg
Author: F.J. Kelly
Author: T. Sandström
Author: A.J. Frew
Author: S.J. Wilson

University divisions

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of https://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×