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Asthma and obesity increase inflammatory markers in children
Harshita Shailesh1, Safa Noor1, Lena Hayati1
1Department of Pediatric Medicine, Division of Pulmonology, Sidra Medicine, Doha, Qatar.
Insights
Asthma and obesity independently increase inflammation in children. Their combined presence alters inflammatory profiles but does not synergistically worsen inflammation, suggesting a moderating effect of obesity.
Area of Science:
- Pediatric immunology
- Inflammation research
- Obesity and respiratory health
Background:
- Asthma and obesity are independently linked to inflammation.
- The combined impact of pediatric asthma and obesity on inflammatory mechanisms requires further investigation.
- Understanding these interactions is crucial for effective treatment strategies.
Purpose of the Study:
- To investigate the interaction effects of asthma and obesity on inflammatory markers in children.
- To assess how co-occurring asthma and obesity influence circulating cytokine and adipokine levels.
- To determine if obesity exacerbates inflammation in children with asthma.
Main Methods:
- Plasma levels of key cytokines (IL-2, IL-5, IL-10, IL-13, IL-17A, IL-22, IL-33, IFN-γ, TNF-α) and leptin were measured using multiplex and singleplex assays.
- The study included four groups of children: normal weight with asthma, overweight/obese with asthma, overweight/obese without asthma, and normal weight without asthma.
- Multiple regression analysis was employed to evaluate independent and interaction effects of asthma and obesity on inflammatory markers.
Main Results:
- Asthma was associated with increased pro-inflammatory cytokines (IL-2, IL-5, IL-13, IL-17A, IL-22, IL-33, TNF-α) and decreased IL-10 and leptin.
- Overweight/obesity correlated with elevated IL-5, IL-17A, IL-22, IL-33, TNF-α, leptin, and reduced IL-10.
- A significant interaction between obesity and asthma was observed for IL-5, IL-10, IL-17A, IL-33, TNF-α, and leptin, but without synergistic amplification of inflammation.
Conclusions:
- Both asthma and obesity independently impact inflammatory profiles in children.
- The concurrent presence of asthma and obesity modifies inflammation but does not lead to a synergistic increase.
- These findings suggest a moderating role of obesity in pediatric asthma-related inflammation, challenging previous assumptions.
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.
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