Obesity-driven airway eosinophilia and neutrophilia in asthma.
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2025-05
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Abstract
Objective
Asthma patients with comorbid obesity tend to have more severe, difficult-to-control asthma than lean asthma patients. This increase in asthma severity may be due, in part, to obesity-related adipokines, such as leptin, which contribute to airway hyperresponsiveness, sustained subclinical chronic inflammation, and treatment resistance. This narrative literature review aims to elucidate the differences in airway eosinophilia and neutrophilia profiles between asthma patients with and without obesity.Methods
A PubMed search of full journal articles published between 1992 and 2024 was performed in April 2024 using the terms "asthma", "tissue eosinophilia" and "obesity" combined with the Boolean operator "AND". Articles detailing airway tissue eosinophilia and neutrophilia in asthma patients or mice were included. Only articles in English were included.Results
To date, several studies have reported increased airway tissue eosinophilia in obese mouse asthma models (four studies) and in asthma patients with obesity (three studies). Airway tissue eosinophilia in asthma patients with obesity is driven by altered and elevated levels of adipokines, pro-inflammatory cytokines, and eosinophil-stimulating chemokines such as eotaxin. Leptin and eotaxin levels are increased in asthma with obesity and contribute to enhanced eosinophil recruitment, migration, adhesion to airway smooth muscles and fibroblasts, and reduced apoptosis.Conclusions
Airway tissue eosinophilia is an important feature of obesity-associated asthma. Airway tissue eosinophilia is mainly driven by obesity-related homeostatic changes. These increased airway tissue eosinophils contribute to a more severe disease.Type
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Zouein, Joseph, Loretta G Que and Jennifer L Ingram (2025). Obesity-driven airway eosinophilia and neutrophilia in asthma. The Journal of asthma : official journal of the Association for the Care of Asthma. pp. 1–11. 10.1080/02770903.2025.2505464 Retrieved from https://hdl.handle.net/10161/32523.
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Scholars@Duke
Loretta Georgina Que
My research interests focus on studying the role of nitric oxide and related enzymes in the pathogenesis of lung disease, specifically that caused by nitrosative/oxidative stress. Proposed studies are performed in cell culture and applied to animal models of disease, then examined in human disease where relevant. It is our hope that by better understanding the role of NO and reactive nitrogen species in mediating inflammation, and regulating cell signaling, that we will not only help to unravel the basic mechanisms of NO related lung disease, but also provide a rationale for targeted therapeutic use of NO.
Key words: nitrosative defense, lung injury, nitric oxide
Jennifer Leigh Ingram
Dr. Ingram's research interests focus on the study of airway remodeling in human asthma. Proliferation, migration, and invasion of airway fibroblasts are key features of airway remodeling that contribute to diminished lung function over time. Dr. Ingram uses molecular biology approaches to define the effects of interleukin-13 (IL-13), a cytokine abundantly produced in the asthmatic airway, in the human airway fibroblast. She has identified important regulatory functions of several proteins prevalent in asthma that control fibroblast growth and pro-fibrotic growth factor production in response to IL-13. By understanding these pathways and their role in human asthma and the chronic effects of airway remodeling, novel treatment strategies may be developed.
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