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Updated: Nov 22, 2025

Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation
Published on: April 3, 2017
Asthma and Obesity: Two Diseases on the Rise and Bridged by Inflammation
Marina Bantulà1,2, Jordi Roca-Ferrer1,2,3, Ebymar Arismendi1,2,3,4
1Department of Internal Medicine, Hospital Clinic, Institut d'Investigació Biomèdica August Pi i Sunyer (IDIBAPS), 08036 Barcelona, Spain.
Insights
Obesity exacerbates asthma through inflammation, with two distinct phenotypes observed. Weight reduction strategies effectively decrease inflammation and improve lung function in asthma patients.
Area of Science:
- Immunology
- Pulmonology
- Metabolic Diseases
Background:
- Asthma and obesity represent significant global health challenges.
- The link between obesity and asthma is complex, involving weight-dependent, causal, genetic, and bidirectional factors.
Purpose of the Study:
- To elucidate the intricate relationship between obesity and asthma.
- To describe the distinct phenotypes of asthma associated with obesity.
- To explore the underlying inflammatory mechanisms linking obesity and asthma.
Main Methods:
- Review of existing literature on obesity-related inflammation and asthma pathogenesis.
- Analysis of the roles of adipose tissue, macrophages, and adipokines in obesity-induced inflammation.
- Examination of pro-inflammatory and anti-inflammatory cytokine pathways in both conditions.
Main Results:
- Obesity is associated with increased pro-inflammatory mediators (leptin, IL-1β, IL-6, TNFα, TGFβ) and M1 macrophage infiltration in adipose tissue.
- Two asthma phenotypes linked to obesity exist: allergic asthma in obese children and late-onset non-allergic asthma.
- Specific cytokines (IL-4, IL-5, IL-13, IL-33) typically associated with asthma may help maintain a lean state.
Conclusions:
- Obesity-related inflammation, driven by adipose tissue dysfunction and specific cytokines, significantly contributes to asthma risk and severity.
- Weight reduction interventions, including diet, exercise, and bariatric surgery, can mitigate inflammation and improve asthma control and lung function.
Abstract:
Asthma and obesity are two epidemics affecting the developed world. The relationship between obesity and both asthma and severe asthma appears to be weight-dependent, causal, partly genetic, and probably bidirectional. There are two distinct phenotypes: 1. Allergic asthma in children with obesity, which worsens a pre-existing asthma, and 2. An often non allergic, late-onset asthma developing as a consequence of obesity. In obesity, infiltration of adipose tissue by macrophages M1, together with an increased expression of multiple mediators that amplify and propagate inflammation, is considered as the culprit of obesity-related inflammation. Adipose tissue is an important source of adipokines, such as pro-inflammatory leptin, produced in excess in obesity, and adiponectin with anti-inflammatory effects with reduced synthesis. The inflammatory process also involves the synthesis of pro-inflammatory cytokines such as IL-1β, IL-6, TNFα, and TGFβ, which also contribute to asthma pathogenesis. In contrast, asthma pro-inflammatory cytokines such as IL-4, IL-5, IL-13, and IL-33 contribute to maintain the lean state. The resulting regulatory effects of the immunomodulatory pathways underlying both diseases have been hypothesized to be one of the mechanisms by which obesity increases asthma risk and severity. Reduction of weight by diet, exercise, or bariatric surgery reduces inflammatory activity and improves asthma and lung function.
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