Asthma and Obesity: Two Diseases on the Rise and Bridged by Inflammation

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, w...

Full description

Bibliographic Details
Main Authors: Marina Bantulà, Jordi Roca-Ferrer, Ebymar Arismendi, César Picado
Format: Article
Language:English
Published: MDPI AG 2021-01-01
Series:Journal of Clinical Medicine
Subjects:
Online Access:https://www.mdpi.com/2077-0383/10/2/169
_version_ 1797542260899840000
author Marina Bantulà
Jordi Roca-Ferrer
Ebymar Arismendi
César Picado
author_facet Marina Bantulà
Jordi Roca-Ferrer
Ebymar Arismendi
César Picado
author_sort Marina Bantulà
collection DOAJ
description 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.
first_indexed 2024-03-10T13:27:12Z
format Article
id doaj.art-89b4066410094d8f9b666bde0d66330b
institution Directory Open Access Journal
issn 2077-0383
language English
last_indexed 2024-03-10T13:27:12Z
publishDate 2021-01-01
publisher MDPI AG
record_format Article
series Journal of Clinical Medicine
spelling doaj.art-89b4066410094d8f9b666bde0d66330b2023-11-21T08:43:37ZengMDPI AGJournal of Clinical Medicine2077-03832021-01-0110216910.3390/jcm10020169Asthma and Obesity: Two Diseases on the Rise and Bridged by InflammationMarina Bantulà0Jordi Roca-Ferrer1Ebymar Arismendi2César Picado3Department of Internal Medicine, Hospital Clinic, Institut d’Investigació Biomèdica August Pi i Sunyer (IDIBAPS), 08036 Barcelona, SpainDepartment of Internal Medicine, Hospital Clinic, Institut d’Investigació Biomèdica August Pi i Sunyer (IDIBAPS), 08036 Barcelona, SpainDepartment of Internal Medicine, Hospital Clinic, Institut d’Investigació Biomèdica August Pi i Sunyer (IDIBAPS), 08036 Barcelona, SpainDepartment of Internal Medicine, Hospital Clinic, Institut d’Investigació Biomèdica August Pi i Sunyer (IDIBAPS), 08036 Barcelona, SpainAsthma 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.https://www.mdpi.com/2077-0383/10/2/169asthmacytokinesphenotypeinflammationobesity
spellingShingle Marina Bantulà
Jordi Roca-Ferrer
Ebymar Arismendi
César Picado
Asthma and Obesity: Two Diseases on the Rise and Bridged by Inflammation
Journal of Clinical Medicine
asthma
cytokines
phenotype
inflammation
obesity
title Asthma and Obesity: Two Diseases on the Rise and Bridged by Inflammation
title_full Asthma and Obesity: Two Diseases on the Rise and Bridged by Inflammation
title_fullStr Asthma and Obesity: Two Diseases on the Rise and Bridged by Inflammation
title_full_unstemmed Asthma and Obesity: Two Diseases on the Rise and Bridged by Inflammation
title_short Asthma and Obesity: Two Diseases on the Rise and Bridged by Inflammation
title_sort asthma and obesity two diseases on the rise and bridged by inflammation
topic asthma
cytokines
phenotype
inflammation
obesity
url https://www.mdpi.com/2077-0383/10/2/169
work_keys_str_mv AT marinabantula asthmaandobesitytwodiseasesontheriseandbridgedbyinflammation
AT jordirocaferrer asthmaandobesitytwodiseasesontheriseandbridgedbyinflammation
AT ebymararismendi asthmaandobesitytwodiseasesontheriseandbridgedbyinflammation
AT cesarpicado asthmaandobesitytwodiseasesontheriseandbridgedbyinflammation