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 hypothesize that pediatric obesity-associated asthma will be characterized by T helper 1(Th1), rather than the Th2 polarization associated with atopic asthma. Moreover, we speculate that Th1 biomarkers and anthropometric measures will correlate with pulmonary function tests (PFTs) in obese asthmatics.

METHODS:We recruited 120 children with 30 in each of the 4 study groups: obese asthmatics, non-obese asthmatics, obese non-asthmatics and non-obese non-asthmatics. All 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-gamma (IFNγ) (Th1) or IL-4 (Th2) within the CD4 population.

RESULTS:Obese asthmatics had significantly higher Th1 responses to PMA (p<0.01) and tetanus toxoid (p<0.05) and lower Th2 responses to PMA (p<0.05) and D. farinae (p<0.01) compared to non-obese asthmatics. Th cell patterns did not differ between obese asthmatics and obese non-asthmatics. Obese asthmatics had lower FEV(1)/FVC (p<0.01) and RV/TLC ratios (p<0.005) compared to the other study groups, which negatively correlated with serum interferon inducible protein-10 (IP-10) and IFNγ levels, respectively. PFTs, however, did not correlate with BMI z-score or waist 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 asthmatics.