Proliferation and inflammation in bronchial epithelium after allergen in atopic asthmatics.

摘要: BACKGROUND: The mechanisms that regulate epithelial integrity and repair in asthma are poorly understood. We hypothesized allergen exposure could alter inflammation, damage proliferation atopic asthma. OBJECTIVE: studied cell infiltration, shedding, expression of the marker Ki-67 cell-cell adhesion molecules Ep-CAM E-cadherin bronchial biopsies 10 mild asthmatics 48 h after experimental diluent (D) (A) challenge a cross-over design. METHODS: Epithelial expressed as percentage not intact epithelium, Ki-67+, eosinophil/EG-2+, CD4+ CD8+ cells were quantified by image analysis analysed semi-quantitatively. RESULTS: shedding was altered A (D: 88.1+/-3.1% vs. A: 89.2+/-3.7%; P=0.63). numbers Ki-67+ 10.2+/-0.2 19.9+/-0.3 cells/mm; P=0.03), EG-2+ 4.3+/-0.5 27+/-0.3 P=0.04) 1.7+/-1.2 12.3+/-0.6 significantly increased A, whilst changed (P>0.05). staining showed similar intensity D found positive correlation between epithelium (Rs: 0.63; P=0.02). CONCLUSION: Our study indicates increases conjunction with inflammation at 2 days exposure. This favours hypothesis long-lasting restitution is involved pathogenesis