Effects of Obesity on Airway and Systemic Inflammation in Asthmatic Children
Emine Vezir1, Ersoy Civelek2, Emine Dibek Misirlioglu2
1Department of Pediatric Allergy and Clinical Immunology, Ankara Health Research and Application Center, University of Health Sciences, Ankara, Turkey, eminevezir@gmail.com.
Insights
This study found no interaction between childhood obesity and asthma regarding airway inflammation. However, interactions were observed in specific inflammatory markers like adiponectin, suggesting a complex relationship in pediatric asthma.
Area of Science:
- Pediatric Pulmonology
- Immunology
- Metabolic Disorders
Background:
- Obesity and asthma represent complex conditions with distinct pediatric phenotypes.
- Limited evidence exists on the pathological interaction between childhood obesity and asthma.
Purpose of the Study:
- To investigate the interaction between obesity and asthma in children.
- To assess airway and systemic inflammation in relation to obesity and asthma.
Main Methods:
- A controlled observational study included 153 children aged 6-18, categorized into four groups: asthma obese (AO), asthma nonobese (ANO), non-asthma obese (NAO), and non-asthma nonobese (NANO).
- Evaluated parameters included spirometry, fractional exhaled nitric oxide (FeNO), skin prick tests, serum inflammatory biomarkers, and sputum inflammatory cells.
- Obesity-asthma interactions were determined through comprehensive analysis of these markers.
Main Results:
- Asthma was independently associated with higher levels of IL-4, IL-5, IL-13, resistin, and YKL-40.
- The asthma obese (AO) group exhibited the lowest adiponectin levels, indicating an obesity-asthma interaction.
- Sputum eosinophilia, neutrophilia, and FeNO levels were elevated in asthmatic patients irrespective of obesity status.
Conclusions:
- No significant interaction was found between childhood obesity and asthma concerning airway inflammation.
- An interaction between obesity and asthma was identified in relation to adiponectin levels and resistin/adiponectin and leptin/adiponectin ratios.
- Serum YKL-40 and resistin levels may be linked to airway inflammation in this pediatric cohort.
Background:
Obese asthma is a complex syndrome with certain phenotypes that differ in children and adults. There is no clear evidence regarding the presence of additive or synergistic pathological interaction between obesity and asthma in children.
Objectives:
Our aim was to demonstrate the interaction of obesity and asthma in children in terms of airway and systemic inflammation by a controlled observational study.
Methods:
Four groups were formed: asthma obese (AO), asthma nonobese (ANO), non-AO (NAO), nonasthma nonobese (NANO). Spirometry test, fractional exhaled nitric oxide (FeNO) test, skin prick test, serum inflammatory biomarkers (C-reactive protein, C3, C4, adiponectin, leptin, resistin, periostin, YKL-40, Type 1, and Type 2 cytokines) were conducted and evaluated in all participants. Sputum inflammatory cells (sputum eosinophils and neutrophils) were evaluated in patients who could produce induced sputum and obesity-asthma interactions were determined.
Results:
A total of 153 participants aged 6-18 years were included in the study, including the AO group (n = 46), the ANO group (n = 45), the NAO group (n = 30), and the NANO group (n = 32). IL-4 (p < 0.001), IL-5 (p < 0.001), IL-13 (p < 0.001), resistin (p < 0.001), and YKL-40 (p < 0.001) levels were higher in patients with asthma independent of obesity. The lowest adiponectin level was found in the AO group and obesity-asthma interaction was detected (p < 0.001). Sputum eosinophilia (p < 0.01), sputum neutrophilia (p < 0.01), and FeNO levels (p = 0.07) were higher in asthmatic patients independent of obesity. In the group with paucigranulocytic inflammation, resistin and YKL-40 levels were significantly lower than in the group without paucigranulocytic inflammation (p < 0.01).
Conclusion:
No interaction was found between obesity and asthma in terms of airway inflammation. Interaction between obesity and asthma was shown in terms of adiponectin level and resistin/adiponectin and leptin/adiponectin ratios. It was found that serum YKL-40 and resistin levels could be associated with airway inflammation.
Related Concept Videos
01:26Asthma-II: Pathophysiology and Classification
Additionally, environmental and genetic factors play crucial roles in determining an individual's susceptibility to asthma and the severity of their condition.
Critical processes in asthma pathophysiology include:
01:20Asthma: Pathogenesis and Management
Asthma is classified as allergic and non-allergic. Allergens such as dust mites, pollen, and pet dander trigger allergic asthma, while factors like cold air, intense emotions, or exercise can induce non-allergic asthma.
01:29Asthma-I: Introduction
01:24Asthma-III: Symptoms and Complications
Classification of Asthma
01:24Obesity
01:30Asthma-IV: Diagnostic and Management
Clinical Assessment for Asthma:
This is the first step in diagnosing and managing asthma. It includes: