Obesity-driven airway eosinophilia and neutrophilia in asthma

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.