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Generation of Lymphocytic Microparticles and Detection of their Proapoptotic Effect on Airway Epithelial Cells
Published on: February 20, 2015
[Airway neutrophils apoptosis in children with severe asthma]
Jing Liao1, Guang-min Nong, Min Jiang
1Department of Pediatrics, the First Affiliated Hospital, Guangxi Medical University, Nanning 530021, China.
Insights
In severe asthma, higher sputum neutrophil counts and elevated IL-8 levels were observed. Suppression of neutrophil apoptosis may contribute to airway inflammation in these patients.
Area of Science:
- Pulmonology
- Immunology
- Cell Biology
Context:
- Severe asthma is characterized by persistent airway inflammation.
- Neutrophils are key inflammatory cells implicated in asthma pathogenesis.
- Understanding neutrophil behavior in severe asthma is crucial for developing targeted therapies.
Purpose:
- To investigate the role of neutrophils and Interleukin-8 (IL-8) in airway inflammation in children with severe asthma.
- To examine the effect of severe asthmatic sputum supernatant on neutrophil apoptosis in vitro.
- To explore potential therapeutic targets by assessing the impact of mifepristone on neutrophil survival.
Summary:
- Children with severe asthma exhibited significantly higher percentages of sputum neutrophils and elevated IL-8 levels in sputum compared to those with mild-moderate asthma and healthy controls.
- In vitro studies demonstrated that sputum supernatant from severe asthmatics, IL-8, and mifepristone suppressed neutrophil apoptosis.
- These findings suggest that impaired neutrophil apoptosis, potentially mediated by IL-8, contributes to neutrophilic airway inflammation in severe asthma.
Impact:
- Provides insights into the mechanisms underlying neutrophilic airway inflammation in severe asthma.
- Highlights IL-8 as a potential biomarker and therapeutic target.
- Suggests that targeting neutrophil apoptosis could be a novel strategy for managing severe asthma.
Objective:
To investigate the changes of neutrophils in airway inflammation in children with severe asthma.
Method:
Children with mild to moderate asthma (n=23), severe asthma (n=16) and healthy control subjects (n=16) underwent lung function tests and sputum induction. The sputum specimens were assayed for cellular differential count, the supernatant and peripheral blood were assayed for the concentrations of IL-8 by "sandwich" enzyme linked immunosorbent assay (ELISA). Sputum supernatant, IL-8 and mifepristone were assessed for their abilities to prolong the in vitro survival of blood-derived neutrophils.
Result:
The percentage of sputum neutrophils was significantly higher in severe asthmatics [59.54 (41.99-74.65)%] than mild-moderate asthmatics [30.03 (15.94-47.71)%] and healthy control subjects [29.72(16.53-45.74)%] (P < 0. 01); the level of IL-8 in sputum was significantly higher in severe asthmatics [2907.78 (331.67 - 3457.93) ng/L] than mild-moderate asthmatics [287.58 (130.75-656.84) ng/L] and healthy control subjects [179.2 (58.55-346.59) ng/L] (P < 0.01); the percentages of neutrophilic apoptosis respectively cultured with LPS [(10.57 +/- 1.97)%], severe asthmatics supernatant [(11.82 +/- 2.96)%], IL-8 [(10.47 +/- 1.93)%], dexamethasone [(9.93 +/- 1.95)%], severe asthma supernatant + mifepristone [(12.15 +/- 2.86)%] in vitro were lower than that cultured with PBS [(17.98 +/- 2.27)%], healthy control supernatant [(17.37 +/- 2.50)%], mild-moderate asthmatics supernatant [(16.35 +/- 3.26)%], mifepristone [(17.89 +/- 2.38)%], and dexamethasone + mifepristone [(17.06 +/- 2.59)%] (P < 0.01).
Conclusion:
Suppression of neutrophilic apoptosis seems to play a potential role in airway neutrophilic inflammation in severe asthmatics, and the level of IL-8 in sputum was significantly higher in patients with severe asthmatics.
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