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Updated: Aug 29, 2026
Methodology for Sputum Induction and Laboratory Processing
Published on: December 17, 2017
[Eosinophils apoptosis in asthmatic children]
Guang-min Nong1, Shu-quan Li, Long Yao
1Department of Pediatrics, The First Affiliated Hospital, Guangxi Medical University, Nanning 530027, China.
Insights
In asthmatic children, eosinophil apoptosis is reduced in airways, but inhaled glucocorticoids increase it. This finding highlights a key mechanism for glucocorticoid therapy in asthma management.
Area of Science:
- Immunology
- Pulmonology
- Cell Biology
Background:
- Eosinophilic airway inflammation is central to asthma pathogenesis.
- Disruptions in eosinophil apoptosis are implicated in asthma mechanisms.
- In vivo studies in adult asthmatics are limited.
Purpose of the Study:
- To investigate the relationship between apoptotic eosinophils and Bcl-2 in children with asthma.
- To examine these factors in vivo within pediatric asthmatic patients.
Main Methods:
- Compared 11 mild-to-moderate asthmatic children (7-14 years) with 7 children with lower respiratory infection.
- Utilized TUNEL and immunohistochemistry to measure apoptotic eosinophils (EG(2)(+)) in sputum, bronchoalveolar lavage (BAL), and bronchial mucosa.
- Assessed Bcl-2 expression in bronchial mucosa before and after inhaled glucocorticoid (GC) treatment.
Main Results:
- Asthmatic children had lower apoptotic EG(2)(+) cells and higher total EG(2)(+) cells in airways compared to controls (P < 0.01, P < 0.001).
- GC treatment increased apoptotic EG(2)(+) cells and decreased total EG(2)(+) cells in asthmatics (P < 0.01).
- FEV(1)% improved post-GC treatment (P < 0.05), correlating positively with eosinophil apoptosis.
Conclusions:
- Eosinophil apoptosis is reduced in the airways of asthmatic children.
- Inducing eosinophil apoptosis is a significant mechanism of inhaled glucocorticoid therapy for asthma.
Unlabelled:
Prominent eosinophil airway inflammation is important in the pathogenesis of asthma. There is increasing evidence that the disorder of eosinophil apoptosis contributes to the mechanism. But most of the studies have been done in vitro or on animal models, very few were done among the adult asthmatics in vivo.
Objective:
The aim of this study was to elucidate the relationship between the apoptotic eosinophils and Bcl-2 in asthmatic children in vivo.
Methods:
Eleven mild to moderate asthmatic patients were recruited and the range of age was 7 - 14 years (9 males, 2 females), meanwhile 7 patients with lower respiratory infection were recruited as control and the range of age was 9 - 14 years (5 males, 2 females). Before and after inhaled glucocorticoid (GC) induced sputum, bronchoalveolar lavage (BAL), bronchial mucosa specimens and peripheral blood were obtained for measuring and comparing the changes of apoptotic EG(2)(+) cell by combining the techniques of TUNEL and immunohistochemistry, meanwhile the expression of Bcl-2 in bronchial mucosa specimens was measured by using the immunohistochemical assay.
Results:
Before the inhalation of GC, the apoptotic EG(2)(+) cells in asthmatics were significantly lower than that in control group (P < 0.01), and the numbers of EG(2)(+) cell in asthmatics group were significantly higher than that in control group (P < 0.001). After the treatment apoptotic EG(2)(+) cells in asthmatics were increased (P < 0.01), and the numbers of EG(2)(+)cell were decreased (P < 0.01, P < 0.05 and P < 0.05, respectively), FEV(1)% was increased (P < 0.05). Before the inhalation of GC, the numbers of Bcl-2(+) cell in asthmatic airway submucosa were higher than that in control group (P < 0.05) but after the treatment the number of Bcl-2(+) cell did not change significantly. (4) Before and after GC treatment the percentages of apoptotic eosinophils of peripheral blood in vivo had no significant changes compared with those of control subjects (P > 0.05). There was a positive correlation between apoptosis of EG(2)(+) cell in sputum, BAL, airway submucosa and FEV(1)% (P < 0.05).
Conclusion:
Apoptosis of EG(2)(+) cell decreased in the airway of asthmatic children and inducing EOS apoptosis is one of the important mechanism of inhaled GC therapy for asthma.
