Ghent University Academic Bibliography

Advanced

United airways: circulating Th2 effector cells in an allergic rhinitis model are responsible for promoting lower airways inflammation

Alex Kleinjan, Monique Willart UGent, Menno van Nimwegen, Karolina Leman, Henk Hoogsteden, Rudy Hendriks and Bart Lambrecht UGent (2010) CLINICAL AND EXPERIMENTAL ALLERGY. 40(3). p.494-504
abstract
Background : Allergic rhinitis (AR) and asthma often coexist and are referred to as 'united airways' disease. However, the molecular and cellular pathways that are crucially involved in the interaction between upper and lower airways remain to be identified. Objective : We sought to assess whether and how AR exacerbates lower airway inflammation upon allergen challenge in mice. Methods : We previously developed an intranasal ovalbumin (OVA)-driven AR model, characterized by nasal eosinophilic inflammation, enhanced serum levels of OVA-specific IgE and Th2 cytokine production in cervical lymph nodes. In OVA-sensitized mice with or without AR, a lower airway challenge was given, and after 24 h, lower airway inflammation was analysed. Results : We found that AR mice were more susceptible to eosinophilic inflammation following a lower airway OVA challenge than OVA-sensitized controls. AR mice manifested increased numbers of eosinophils in bronchoalveolar lavage fluid and increased inter-cellular adhesion molecule-1 (ICAM-1) expression on lung endothelium, when compared with OVA-sensitized controls. Depletion of T cells in OVA-challenged AR mice completely abrogated all hallmarks of lower airway inflammation, including enhanced IL-5 and tissue eosinophilia. Conversely, adoptive transfer of Th2 effector cells in naive animals induced lower airway eosinophilic inflammation after challenge with OVA. Blocking T cell recirculation during AR development by the spingosine-1 analogue FTY720 also prevented lower airway inflammation including ICAM-1 expression in AR mice upon a single lower airway challenge. Conclusion : Our mouse model of 'united airways' disease supports epidemiological and clinical data that AR has a significant impact on lower airway inflammation. Circulating Th2 effector cells are responsible for lung priming in AR mice, most likely through up-regulation of ICAM-1.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
Th2 cells, allergic rhinitis, asthma, ICAM-1, mouse model, DENDRITIC CELLS, EOSINOPHILIC INFLAMMATION, PULMONARY EOSINOPHILIA, ADHESION MOLECULE-1, MURINE MODEL, MAST-CELLS, T-CELLS, ASTHMA, LUNG, ACCUMULATION
journal title
CLINICAL AND EXPERIMENTAL ALLERGY
Clin. Exp. Allergy
volume
40
issue
3
pages
494 - 504
Web of Science type
Article
Web of Science id
000274388300019
JCR category
ALLERGY
JCR impact factor
4.195 (2010)
JCR rank
3/20 (2010)
JCR quartile
1 (2010)
ISSN
0954-7894
DOI
10.1111/j.1365-2222.2009.03417.x
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
833714
handle
http://hdl.handle.net/1854/LU-833714
date created
2010-01-22 10:02:59
date last changed
2012-11-07 15:03:07
@article{833714,
  abstract     = {Background : Allergic rhinitis (AR) and asthma often coexist and are referred to as 'united airways' disease. However, the molecular and cellular pathways that are crucially involved in the interaction between upper and lower airways remain to be identified. 
Objective : We sought to assess whether and how AR exacerbates lower airway inflammation upon allergen challenge in mice. 
Methods : We previously developed an intranasal ovalbumin (OVA)-driven AR model, characterized by nasal eosinophilic inflammation, enhanced serum levels of OVA-specific IgE and Th2 cytokine production in cervical lymph nodes. In OVA-sensitized mice with or without AR, a lower airway challenge was given, and after 24 h, lower airway inflammation was analysed. 
Results : We found that AR mice were more susceptible to eosinophilic inflammation following a lower airway OVA challenge than OVA-sensitized controls. AR mice manifested increased numbers of eosinophils in bronchoalveolar lavage fluid and increased inter-cellular adhesion molecule-1 (ICAM-1) expression on lung endothelium, when compared with OVA-sensitized controls. Depletion of T cells in OVA-challenged AR mice completely abrogated all hallmarks of lower airway inflammation, including enhanced IL-5 and tissue eosinophilia. Conversely, adoptive transfer of Th2 effector cells in naive animals induced lower airway eosinophilic inflammation after challenge with OVA. Blocking T cell recirculation during AR development by the spingosine-1 analogue FTY720 also prevented lower airway inflammation including ICAM-1 expression in AR mice upon a single lower airway challenge. 
Conclusion : Our mouse model of 'united airways' disease supports epidemiological and clinical data that AR has a significant impact on lower airway inflammation. Circulating Th2 effector cells are responsible for lung priming in AR mice, most likely through up-regulation of ICAM-1.},
  author       = {Kleinjan, Alex and Willart, Monique and van Nimwegen, Menno and Leman, Karolina and Hoogsteden, Henk and Hendriks, Rudy and Lambrecht, Bart},
  issn         = {0954-7894},
  journal      = {CLINICAL AND EXPERIMENTAL ALLERGY},
  keyword      = {Th2 cells,allergic rhinitis,asthma,ICAM-1,mouse model,DENDRITIC CELLS,EOSINOPHILIC INFLAMMATION,PULMONARY EOSINOPHILIA,ADHESION MOLECULE-1,MURINE MODEL,MAST-CELLS,T-CELLS,ASTHMA,LUNG,ACCUMULATION},
  language     = {eng},
  number       = {3},
  pages        = {494--504},
  title        = {United airways: circulating Th2 effector cells in an allergic rhinitis model are responsible for promoting lower airways inflammation},
  url          = {http://dx.doi.org/10.1111/j.1365-2222.2009.03417.x},
  volume       = {40},
  year         = {2010},
}

Chicago
Kleinjan, Alex, Monique Willart, Menno van Nimwegen, Karolina Leman, Henk Hoogsteden, Rudy Hendriks, and Bart Lambrecht. 2010. “United Airways: Circulating Th2 Effector Cells in an Allergic Rhinitis Model Are Responsible for Promoting Lower Airways Inflammation.” Clinical and Experimental Allergy 40 (3): 494–504.
APA
Kleinjan, Alex, Willart, M., van Nimwegen, M., Leman, K., Hoogsteden, H., Hendriks, R., & Lambrecht, B. (2010). United airways: circulating Th2 effector cells in an allergic rhinitis model are responsible for promoting lower airways inflammation. CLINICAL AND EXPERIMENTAL ALLERGY, 40(3), 494–504.
Vancouver
1.
Kleinjan A, Willart M, van Nimwegen M, Leman K, Hoogsteden H, Hendriks R, et al. United airways: circulating Th2 effector cells in an allergic rhinitis model are responsible for promoting lower airways inflammation. CLINICAL AND EXPERIMENTAL ALLERGY. 2010;40(3):494–504.
MLA
Kleinjan, Alex, Monique Willart, Menno van Nimwegen, et al. “United Airways: Circulating Th2 Effector Cells in an Allergic Rhinitis Model Are Responsible for Promoting Lower Airways Inflammation.” CLINICAL AND EXPERIMENTAL ALLERGY 40.3 (2010): 494–504. Print.