Abstract
Background: The mechanisms that regulate epithelial integrity and repair in asthma are poorly understood. We hypothesized that allergen exposure could alter epithelial inflammation, damage and proliferation in atopic asthma. Objective: We studied epithelial cell infiltration, shedding, expression of the proliferation marker Ki-67 and the epithelial cell-cell adhesion molecules Ep-CAM and E-cadherin in bronchial biopsies of 10 atopic mild asthmatics 48 h after experimental diluent (D) and allergen (A) challenge in a crossover design. Methods: Epithelial shedding, expressed as percentage of not intact epithelium, Ki-67+, eosinophil/EG-2+, CD4+ and CD8+ cells were quantified by image analysis in bronchial epithelium, and adhesion molecules were analysed semi-quantitatively. Results: Epithelial shedding was not altered by A (D: 88.1 ± 3.1% vs. A: 89.2 ± 3.7%; P = 0.63). The numbers of Ki-67+ epithelial (D: 10.2 ± 0.2 vs. A: 19.9±0.3 cells/mm; P= 0.03), EG-2+ (D: 4.3±0.5 vs. A: 27±0.3 cells/mm; P = 0.04) and CD4+ cells (D: 1.7 ± 1.2 vs. A: 12.3 ± 0.6 cells/mm; P = 0.04) were significantly increased after A, whilst CD8+ numbers were not significantly changed (P>0.05). E-cadherin and Ep-CAM epithelial staining showed a similar intensity after D and A (P>0.05). We found a positive correlation between EG-2+ and Ki-67+ cells in the epithelium (Rs: 0.63; P = 0.02). Conclusion: Our study indicates that allergen challenge increases epithelial proliferation in conjunction with inflammation at 2 days after exposure. This favours the hypothesis that long-lasting epithelial restitution is involved in the pathogenesis of asthma.
| Original language | English |
|---|---|
| Pages (from-to) | 905-911 |
| Number of pages | 7 |
| Journal | Clinical and Experimental Allergy |
| Volume | 33 |
| Issue number | 7 |
| DOIs | |
| Publication status | Published - Jul 1 2003 |
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Keywords
- Asthma
- Epithelium
- Proliferation and inflammation
ASJC Scopus subject areas
- Immunology
Cite this
Proliferation and inflammation in bronchial epithelium after allergen in atopic asthmatics. / Ricciardolo, Fabio L M; Di Stefano, A.; Van Krieken, J. H J M; Sont, J. K.; Van Schadewijk, A.; Rabe, K. F.; Donner, C. F.; Hiemstra, P. S.; Sterk, P. J.; Mauad, T.
In: Clinical and Experimental Allergy, Vol. 33, No. 7, 01.07.2003, p. 905-911.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Proliferation and inflammation in bronchial epithelium after allergen in atopic asthmatics
AU - Ricciardolo, Fabio L M
AU - Di Stefano, A.
AU - Van Krieken, J. H J M
AU - Sont, J. K.
AU - Van Schadewijk, A.
AU - Rabe, K. F.
AU - Donner, C. F.
AU - Hiemstra, P. S.
AU - Sterk, P. J.
AU - Mauad, T.
PY - 2003/7/1
Y1 - 2003/7/1
N2 - Background: The mechanisms that regulate epithelial integrity and repair in asthma are poorly understood. We hypothesized that allergen exposure could alter epithelial inflammation, damage and proliferation in atopic asthma. Objective: We studied epithelial cell infiltration, shedding, expression of the proliferation marker Ki-67 and the epithelial cell-cell adhesion molecules Ep-CAM and E-cadherin in bronchial biopsies of 10 atopic mild asthmatics 48 h after experimental diluent (D) and allergen (A) challenge in a crossover design. Methods: Epithelial shedding, expressed as percentage of not intact epithelium, Ki-67+, eosinophil/EG-2+, CD4+ and CD8+ cells were quantified by image analysis in bronchial epithelium, and adhesion molecules were analysed semi-quantitatively. Results: Epithelial shedding was not altered by A (D: 88.1 ± 3.1% vs. A: 89.2 ± 3.7%; P = 0.63). The numbers of Ki-67+ epithelial (D: 10.2 ± 0.2 vs. A: 19.9±0.3 cells/mm; P= 0.03), EG-2+ (D: 4.3±0.5 vs. A: 27±0.3 cells/mm; P = 0.04) and CD4+ cells (D: 1.7 ± 1.2 vs. A: 12.3 ± 0.6 cells/mm; P = 0.04) were significantly increased after A, whilst CD8+ numbers were not significantly changed (P>0.05). E-cadherin and Ep-CAM epithelial staining showed a similar intensity after D and A (P>0.05). We found a positive correlation between EG-2+ and Ki-67+ cells in the epithelium (Rs: 0.63; P = 0.02). Conclusion: Our study indicates that allergen challenge increases epithelial proliferation in conjunction with inflammation at 2 days after exposure. This favours the hypothesis that long-lasting epithelial restitution is involved in the pathogenesis of asthma.
AB - Background: The mechanisms that regulate epithelial integrity and repair in asthma are poorly understood. We hypothesized that allergen exposure could alter epithelial inflammation, damage and proliferation in atopic asthma. Objective: We studied epithelial cell infiltration, shedding, expression of the proliferation marker Ki-67 and the epithelial cell-cell adhesion molecules Ep-CAM and E-cadherin in bronchial biopsies of 10 atopic mild asthmatics 48 h after experimental diluent (D) and allergen (A) challenge in a crossover design. Methods: Epithelial shedding, expressed as percentage of not intact epithelium, Ki-67+, eosinophil/EG-2+, CD4+ and CD8+ cells were quantified by image analysis in bronchial epithelium, and adhesion molecules were analysed semi-quantitatively. Results: Epithelial shedding was not altered by A (D: 88.1 ± 3.1% vs. A: 89.2 ± 3.7%; P = 0.63). The numbers of Ki-67+ epithelial (D: 10.2 ± 0.2 vs. A: 19.9±0.3 cells/mm; P= 0.03), EG-2+ (D: 4.3±0.5 vs. A: 27±0.3 cells/mm; P = 0.04) and CD4+ cells (D: 1.7 ± 1.2 vs. A: 12.3 ± 0.6 cells/mm; P = 0.04) were significantly increased after A, whilst CD8+ numbers were not significantly changed (P>0.05). E-cadherin and Ep-CAM epithelial staining showed a similar intensity after D and A (P>0.05). We found a positive correlation between EG-2+ and Ki-67+ cells in the epithelium (Rs: 0.63; P = 0.02). Conclusion: Our study indicates that allergen challenge increases epithelial proliferation in conjunction with inflammation at 2 days after exposure. This favours the hypothesis that long-lasting epithelial restitution is involved in the pathogenesis of asthma.
KW - Asthma
KW - Epithelium
KW - Proliferation and inflammation
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UR - http://www.scopus.com/inward/citedby.url?scp=0038500698&partnerID=8YFLogxK
U2 - 10.1046/j.1365-2222.2003.01686.x
DO - 10.1046/j.1365-2222.2003.01686.x
M3 - Article
VL - 33
SP - 905
EP - 911
JO - Clinical and Experimental Allergy
JF - Clinical and Experimental Allergy
SN - 0954-7894
IS - 7
ER -