Zouein Joseph, Que Loretta G, Ingram Jennifer L
Department of Medicine, Duke University School of Medicine, Durham, NC, USA.
Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, Duke University School of Medicine, Durham, NC, USA.
J Asthma. 2025 May 19:1-11. doi: 10.1080/02770903.2025.2505464.
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.
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.
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.
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.
合并肥胖症的哮喘患者往往比体型偏瘦的哮喘患者患有更严重、更难控制的哮喘。哮喘严重程度的增加可能部分归因于与肥胖相关的脂肪因子，如瘦素，它会导致气道高反应性、持续性亚临床慢性炎症和治疗抵抗。这篇叙述性文献综述旨在阐明肥胖和非肥胖哮喘患者气道嗜酸性粒细胞增多和中性粒细胞增多情况的差异。
2024年4月，使用“哮喘”“组织嗜酸性粒细胞增多”和“肥胖”等术语，并结合布尔运算符“AND”，在PubMed上搜索1992年至2024年间发表的全文期刊文章。纳入详细描述哮喘患者或小鼠气道组织嗜酸性粒细胞增多和中性粒细胞增多情况的文章。仅纳入英文文章。
迄今为止，多项研究报告称，在肥胖小鼠哮喘模型（四项研究）和肥胖哮喘患者（三项研究）中，气道组织嗜酸性粒细胞增多。肥胖哮喘患者的气道组织嗜酸性粒细胞增多是由脂肪因子、促炎细胞因子和嗜酸性粒细胞刺激趋化因子（如嗜酸性粒细胞趋化因子）水平的改变和升高所驱动的。肥胖哮喘患者的瘦素和嗜酸性粒细胞趋化因子水平升高，有助于增强嗜酸性粒细胞的募集、迁移、与气道平滑肌和成纤维细胞的黏附，并减少细胞凋亡。
气道组织嗜酸性粒细胞增多是肥胖相关性哮喘的一个重要特征。气道组织嗜酸性粒细胞增多主要由肥胖相关的稳态变化驱动。这些气道组织嗜酸性粒细胞增多会导致病情更严重。
