Asthma and obesity increase inflammatory markers in children.

IF 3.3 Q2 ALLERGY
Frontiers in allergy Pub Date : 2025-01-20 eCollection Date: 2024-01-01 DOI:10.3389/falgy.2024.1536168
Harshita Shailesh, Safa Noor, Lena Hayati, Antonisamy Belavendra, Nicholas Van Panhuys, Abdul Badi Abou-Samra, Stefan Worgall, Ibrahim Janahi
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Abstract

Background: Asthma and obesity are both characterized by inflammation. However, the combined impact of these conditions on inflammatory mechanisms in children has not been studied extensively. To address this gap, we investigated the interaction effects of asthma and obesity on inflammation in children.

Methods: The multiplex and singleplex assays were used to measure the levels of circulating cytokines, including IL-2, IL-5, IL-10, IL-13, IL-17A, IL-22, IL-33, IFN-γ, TNF-α, and the adipokine leptin, in plasma. The study included 97 children with normal weight and asthma (NW-A), 100 children with overweight/obesity and asthma (OO-A), 100 with overweight/obesity and no asthma (OO), and 67 normal weight children and no asthma (NW). The independent effects of asthma, obesity, and their interaction effect on these inflammatory markers were assessed using multiple regression analysis.

Results: Asthma was associated with the increased expression of pro-inflammatory cytokines, including IL-2, IL-5, IL-13, IL-17A, IL-22, IL-33, and TNF-α, and reduced levels of anti-inflammatory cytokine, IL-10 and adipokine, leptin in the circulation. Overweight/obesity was also linked to increased plasma levels of IL-5, IL-17A, IL-22, IL-33, TNF-α, and leptin and decreased levels of IL-10. In addition, obesity and asthma showed a significant interaction effect on the plasma levels of IL-5, IL-10, IL-17A, IL-33, TNF-α, and leptin. However, the interaction did not result in a synergistic or additive impact on cytokines, indicating a moderating effect of obesity on inflammation in pediatric asthma.

Conclusion: Both asthma and overweight/obesity were independently associated with increased expression of pro-inflammatory cytokines and decreased expression of anti-inflammatory cytokine in children. While the concurrent presence of asthma and obesity altered the inflammatory profile, it did not synergistically amplify the inflammation. These findings challenge the previous view that obesity enhances inflammation in individuals with asthma and highlight the importance of considering both conditions while treating obesity-associated asthma in children. Future studies are necessary to further explore the mechanisms that link obesity and asthma in the pediatric population.

哮喘和肥胖会增加儿童的炎症标志物。
背景:哮喘和肥胖都以炎症为特征。然而,这些条件对儿童炎症机制的综合影响尚未得到广泛研究。为了解决这一差距,我们研究了哮喘和肥胖对儿童炎症的相互作用。方法:采用复形法和单形法测定血浆中循环细胞因子IL-2、IL-5、IL-10、IL-13、IL-17A、IL-22、IL-33、IFN-γ、TNF-α和脂肪因子瘦素水平。研究对象为97例体重正常且哮喘儿童(NW- a), 100例超重/肥胖且哮喘儿童(OO- a), 100例超重/肥胖且无哮喘儿童(OO), 67例体重正常且无哮喘儿童(NW)。使用多元回归分析评估哮喘、肥胖的独立影响及其对这些炎症标志物的相互作用。结果:哮喘与促炎细胞因子IL-2、IL-5、IL-13、IL-17A、IL-22、IL-33、TNF-α表达升高,循环中抗炎细胞因子IL-10、脂肪因子、瘦素水平降低有关。超重/肥胖还与血浆中IL-5、IL-17A、IL-22、IL-33、TNF-α和瘦素水平升高以及IL-10水平降低有关。此外,肥胖和哮喘对血浆中IL-5、IL-10、IL-17A、IL-33、TNF-α和瘦素水平有显著的交互作用。然而,这种相互作用并没有导致对细胞因子的协同或附加影响,这表明肥胖对儿童哮喘炎症的调节作用。结论:儿童哮喘和超重/肥胖均与促炎细胞因子表达升高和抗炎细胞因子表达降低独立相关。虽然哮喘和肥胖的同时存在改变了炎症特征,但它并没有协同放大炎症。这些发现挑战了先前的观点,即肥胖会增加哮喘患者的炎症,并强调了在治疗儿童肥胖相关哮喘时考虑这两种情况的重要性。未来的研究需要进一步探索儿童肥胖和哮喘之间的联系机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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CiteScore
2.80
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