Association of leptin with disease severity and inflammation indicators in Chinese obese children with allergic rhinitis. Issue 2 (25th January 2018)

• Record Type: Journal Article
• Authors: Liu, Wenlong; Zeng, Qingxiang; Zhou, Lifeng; Luo, Renzhong; Dong, Haipeng
• Is Part Of: Pediatric allergy and immunology. Volume 29:Issue 2(2018)
• Page Start: 186
• Page End: 193
• Publication Date: 2018-01-25
• Subjects: allergic rhinitis -- children -- leptin -- obesity; Allergy in children -- Periodicals; Immunologic diseases in children -- Periodicals; 617
• DOI: 10.1111/pai.12856
• Languages: English
• ISSNs: 0905-6157

Abstract

Abstract: Background: The prevalence of both obesity and allergic diseases in children has increased over the last several decades. However, the direct relationship between diverse allergic diseases and obesity has varied in different studies. Therefore, we aimed to examine the effect of obesity on the incidence and severity of allergic rhinitis (AR) and the possible key inflammation mediators during AR. Methods: A total of 3126 healthy students (without chronic diseases) were recruited from 14 randomly selected secondary schools in Guangzhou, China. Body mass index (BMI), waist circumference (WC), waist‐to‐height ratio (WHR), and body fat percentage (PBF) were measured and compared. The effect of obesity indicators and leptin level (exposures) on the incidence (primary outcome) and severity of AR (secondary outcomes) was analyzed. Inflammatory markers were detected and compared among groups. Results: The symptom score (9.5 ± 3.1 vs 8.2 ± 3.5, P < .05) and medication score (3.6 ± 1.6 vs 2.9 ± 1.8, P < .05) were significantly higher in obese children with AR than in non‐obese children with AR. After adjusting for potential confounders, multiple linear regression analysis showed that the serum leptin concentration was significantly correlated with the levels of T‐helper (TH) 2 cytokines (coefficient, 0.48 [95% CI, 0.05‐0.91]), TH17 cytokines (coefficient, 0.39 [95% CI, 0.11‐0.89]), and regulatory T‐cell cytokines (IL‐10, coefficient, −0.43 [95% CI, −0.02‐0.65]; TGF‐β, coefficient, −0.65 [95% CI, −0.06‐1.35]) in patients with AR. Conclusions: Our study shows that obesity exacerbates inflammation and contributes to disease severity in AR. Our study provides evidence that leptin was involved in enhanced TH inflammation as well as the accumulation and activation of inflammatory cells in obese children with AR. Abstract :