The Journal of asthma : official journal of the Association for the Care of Asthma · 2011
Epithelial apoptosis and loss in airways of children with asthma.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
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Ошибки и ограничения
История · было → стало
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Zhou Chunju, Yin Genquan, Liu Jinrong, Liu Xicheng, Zhao Shunying
Аннотация
OBJECTIVE: To examine loss and apoptosis of bronchial epithelial cells in children with asthma.
METHODS: We examined endobronchial biopsies from 13 asthmatic children and 11 non-asthmatic control subjects with other respiratory diseases. Postmortem samples were obtained from six children who died from non-respiratory diseases. We examined bronchial epithelial shedding by morphology; expression of caspase-3 and terminal deoxynucleotidyl-mediated dUTP nick end labeling (TUNEL) were used to study bronchial epithelial apoptosis.
RESULTS: We found epithelial loss to be increased in asthmatic children compared with non-asthmatic control subjects (p = .001) and postmortem children (p = .001). Caspase-3(+) epithelial cells were significantly greater in children with asthma compared with both non-asthmatic control subjects (p = .001) and the postmortem group (p = .002); TUNEL(+) epithelial cells were also increased in columnar cells in the asthmatic children compared with the non-asthmatic control subjects (p = .002) and the postmortem group (p = .001). Eosinophilia was absent in 11 of 13 asthmatic children, although they tended to have submucosal lymphocyte infiltration. Smooth muscle and mucus gland hyperplasia were seen in some asthmatic children whose biopsy specimens included these structures. Basement membranes of childhood asthmatics were thicker than in non-asthmatic controls (p = .002) and postmortem subjects (p = .001).
CONCLUSION: Generally, apoptosis and loss of bronchial epithelial cells were increased in childhood asthma; increased apoptosis might be related to epithelial loss.
METHODS: We examined endobronchial biopsies from 13 asthmatic children and 11 non-asthmatic control subjects with other respiratory diseases. Postmortem samples were obtained from six children who died from non-respiratory diseases. We examined bronchial epithelial shedding by morphology; expression of caspase-3 and terminal deoxynucleotidyl-mediated dUTP nick end labeling (TUNEL) were used to study bronchial epithelial apoptosis.
RESULTS: We found epithelial loss to be increased in asthmatic children compared with non-asthmatic control subjects (p = .001) and postmortem children (p = .001). Caspase-3(+) epithelial cells were significantly greater in children with asthma compared with both non-asthmatic control subjects (p = .001) and the postmortem group (p = .002); TUNEL(+) epithelial cells were also increased in columnar cells in the asthmatic children compared with the non-asthmatic control subjects (p = .002) and the postmortem group (p = .001). Eosinophilia was absent in 11 of 13 asthmatic children, although they tended to have submucosal lymphocyte infiltration. Smooth muscle and mucus gland hyperplasia were seen in some asthmatic children whose biopsy specimens included these structures. Basement membranes of childhood asthmatics were thicker than in non-asthmatic controls (p = .002) and postmortem subjects (p = .001).
CONCLUSION: Generally, apoptosis and loss of bronchial epithelial cells were increased in childhood asthma; increased apoptosis might be related to epithelial loss.