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Generation of Lymphocytic Microparticles and Detection of their Proapoptotic Effect on Airway Epithelial Cells
Published on: February 20, 2015
Epithelial apoptosis and loss in airways of children with asthma
Chunju Zhou1, Genquan Yin, Jinrong Liu
1Department of Pathology, Beijing Children's Hospital Affiliated to Capital Medical University, Beijing, PR China.
Insights
Childhood asthma is linked to increased bronchial epithelial cell loss and apoptosis. This cell death may explain the observed epithelial loss in young asthma patients.
Area of Science:
- Pulmonary Medicine
- Cell Biology
- Pediatrics
Background:
- Childhood asthma involves airway inflammation and remodeling.
- Epithelial cell integrity is crucial for airway health.
Purpose of the Study:
- To investigate bronchial epithelial cell loss and apoptosis in children with asthma.
- To correlate these findings with asthma pathology.
Main Methods:
- Analysis of endobronchial biopsies from asthmatic children, non-asthmatic controls, and postmortem samples.
- Morphological assessment of epithelial shedding.
- Immunohistochemical staining for caspase-3 and TUNEL assay for apoptosis.
Main Results:
- Increased epithelial loss and apoptosis (caspase-3 and TUNEL positive cells) in asthmatic children compared to controls.
- Thicker basement membranes observed in childhood asthmatics.
- Submucosal lymphocyte infiltration noted, with absence of eosinophilia in most cases.
Conclusions:
- Childhood asthma exhibits elevated bronchial epithelial cell apoptosis and loss.
- Increased apoptosis is a potential mechanism contributing to epithelial loss in pediatric asthma.
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.
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