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Assessment of Child Anthropometry in a Large Epidemiologic Study
Published on: February 2, 2017
Obesity-associated asthma in children: a distinct entity
Deepa Rastogi1, Stephen M Canfield2, Andrea Andrade1
1Department of Pediatrics, Albert Einstein College of Medicine, Bronx.
Insights
Pediatric asthma in obese children shows a T helper 1 (Th1) immune response, unlike typical atopic asthma. This Th1 polarization is linked to poorer lung function in obese children with asthma.
Area of Science:
- Immunology
- Pediatrics
- Respiratory Medicine
Background:
- Obesity-associated asthma is a distinct clinical entity in children.
- Mechanisms involve obesity-mediated inflammation and adiposity, poorly defined in pediatric populations.
- Hypothesized a T helper 1 (Th1) immune response, contrasting with Th2 in atopic asthma.
Purpose of the Study:
- To investigate immune differences in pediatric obesity-associated asthma.
- To explore the relationship between Th1/Th2 biomarkers, anthropometry, and pulmonary function in obese asthmatic children.
Main Methods:
- Recruited 120 children across four groups: obese asthmatic, nonobese asthmatic, obese nonasthmatic, and nonobese nonasthmatic.
- Conducted pulmonary function testing (PFTs) and measured serum cytokines.
- Analyzed T-cell responses for intracellular interferon-γ (IFN-γ) (Th1) and IL-4 (Th2) via flow cytometry.
Main Results:
- Obese asthmatic children exhibited significantly higher Th1 responses and lower Th2 responses compared to nonobese asthmatic children.
- Th-cell patterns were similar between obese asthmatic and obese nonasthmatic children.
- Obese asthmatic children showed reduced FEV1/FVC and RV/TLC ratios, correlating with serum IFN-γ levels.
Conclusions:
- Pediatric obesity-associated asthma is characterized by Th1 immune polarization, differentiating it from atopic asthma.
- The altered immune environment in obese asthmatic children inversely correlates with pulmonary function.
Background:
Obesity-associated asthma has been proposed to be a distinct entity, differing in immune pathogenesis from atopic asthma. Both obesity-mediated inflammation and increase in adiposity are potential mechanistic factors that are poorly defined among children. We hypothesized that pediatric obesity-associated asthma would be characterized by T helper (Th) 1, rather than the Th2 polarization associated with atopic asthma. Moreover, we speculated that Th1 biomarkers and anthropometric measures would correlate with pulmonary function tests (PFTs) in obese asthmatic children.
Methods:
We recruited 120 children, with 30 in each of the four study groups: obese asthmatic children, nonobese asthmatic children, obese nonasthmatic children, and nonobese nonasthmatic children. All children underwent pulmonary function testing. Blood was collected for measurement of serum cytokines. T-cell responses to mitogen, phorbol 12-myristate 13-acetate (PMA), or antigens tetanus toxoid or Dermatophagoides farinae were obtained by flow cytometric analysis of intracellular cytokine staining for interferon-γ (IFN-γ) (Th1) or IL-4 (Th2) within the CD4 population.
Results:
Obese asthmatic children had significantly higher Th1 responses to PMA (P < .01) and tetanus toxoid (P < .05) and lower Th2 responses to PMA (P < .05) and D farinae (P < .01) compared with nonobese asthmatic children. Th-cell patterns did not differ between obese asthmatic children and obese nonasthmatic children. Obese asthmatic children had lower FEV(1)/FVC (P < .01) and residual volume/total lung capacity ratios (P < .005) compared with the other study groups, which negatively correlated with serum interferon-inducible protein 10 and IFN-γ levels, respectively. PFTs, however, did not correlate with BMI z score or waist to hip ratio.
Conclusions:
We found that pediatric obesity-associated asthma differed from atopic asthma and was characterized by Th1 polarization. The altered immune environment inversely correlated with PFTs in obese asthmatic children.
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