期刊
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
卷 165, 期 2, 页码 266-272出版社
AMER THORACIC SOC
DOI: 10.1164/ajrccm.165.2.2101069
关键词
bronchial asthma; respiratory epithelium; fibroblasts; bronchial allergen challenge; endobronchial challenge tests
资金
- NHLBI NIH HHS [HL67663, HL03663] Funding Source: Medline
- NIAID NIH HHS [AI24509] Funding Source: Medline
- NIEHS NIH HHS [ES05721] Funding Source: Medline
- NIGMS NIH HHS [GM08562] Funding Source: Medline
Epithelial injury and subepithelial collagen deposition are characteristic of asthma. We hypothesized that epithelial cell proliferation increases after airway injury in asthmatics, that epithelial cells stimulate lung myofibroblast collagen production, and that both processes are modulated by allergen-recruited inflammatory cells. Epithelial cells obtained at baseline, I cl, and I and 2 wk after endobronchial allergen challenge from asthmatics and nonasthmatics were placed in culture, with and without bronchoalveolar lavage cells obtained from the same segment. Epithelial cell proliferation and collagen synthesis by human lung myofibroblasts stimulated with culture medium from these epithelial cells were determined. Epithelial proliferation increased (108 50% above baseline, p = 0.01 for cl, and p = 0.004 for group X day interaction) I wk post-challenge in cells from asthmatics, but not from nonasthmatics, and required bronchoalveolar lavage cell coculture. Culture medium from epithelium harvested from asthmatics, but not from nonasthmatics at I to 2 wk postchallenge stimulated collagen type III production 50% to 70% (p = 0.043 for clinical group, p = 0.012 for day, and p = 0.022 for group X day interaction), but not collagen type I. This effect was independent of an acute eosinophilic response. We conclude that epithelial cells from asthmatics, but not from nonasthmatics, are stimulated to proliferate after allergen challenge, and over 1 to 2 wk postchallenge, stimulate collagen type III synthesis by lung myofibroblasts. Epithelial cell proliferation appears dependent upon infiltrating inflammatory cells, but stimulation of collagen type III does not.
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