Yayınlanmış 1 Ocak 2021
| Sürüm v1
Dergi makalesi
Açık
Effects of Obesity on Airway and Systemic Inflammation in Asthmatic Children
Oluşturanlar
- 1. Univ Hlth Sci, Ankara Hlth Res & Applicat Ctr, Dept Pediat Allergy & Clin Immunol, Ankara, Turkey
- 2. Univ Hlth Sci, Ankara Childrens Hematol Oncol Training & Res Hos, Dept Pediat Allergy & Clin Immunol, Ankara, Turkey
- 3. Ankara Childrens Hematol Oncol Training & Res Hos, Dept Pathol, Ankara, Turkey
- 4. Ihsan Dogramaci Bilkent Univ, Sci Fac, Dept Mol Biol & Genet, Ankara, Turkey
- 5. Ankara Childrens Hematol Oncol Training & Res Hos, Dept Histol, Ankara, Turkey
- 6. Ankara Childrens Hematol Oncol Training & Res Hos, Dept Pediat Endocrinol, Ankara, Turkey
- 7. Mugla Sitki Kocman Univ, Dept Pediat Allergy & Immunol, Fac Med, Mugla, Turkey
Açıklama
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.
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