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

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.

Precision Medicine for Paediatric Severe Asthma: Current Status and Future Direction

“…Important comorbidities include dysfunctional breathing, 27 allergic rhinitis, 28 sinusitis, 29 anxiety and depression, 30 and obesity. 31 The evidence however suggests that treatment of allergic rhinitis does not improve asthma symptoms in either children or adults where both conditions co-exist. 32 Home visits are important because they allow the asthma team to get an impression of the home environment.…”

Leptin and TGF-β1 Downregulate PREP1 Expression in Human Adipose-Derived Mesenchymal Stem Cells and Mature Adipocytes

“…In this context, a previous study suggested that IL-33 is produced by M2 macrophages, which sustain adipose tissue homeostasis. Interestingly, IL-33 contributes to maintain the lean state through the activation of anti-inflammatory M2 macrophages, and in humans, low serum IL-33 levels are associated with high BMI (Liew et al, 2016;Bantulà et al, 2021).…”

“…IL-33 is able to counter excessive inflammation in adipose tissue responses by targeting immune cells expressing the receptor suppression of tumorigenicity 2 receptor (ST2) for IL-33. Furthermore, mice lacking ST2 or IL-33 develop increased adiposity and worsened metabolic profiles, as well as IL-33 treatment triggers the expansion of a group of Fox3 + ST2 + Tregs and attenuates adipose tissue inflammation ( Bantulà et al, 2021 ). Moreover, the metabolic activity of the epicardial adipose tissue is associated with elevated IL-33 ( Gruzdeva et al, 2018 ).…”

Evaluation of the obesity influence on the life quality in patients with bronchial asthma

“…In turn, the number of asthma patients in combination with obesity is growing, which is associated with an increase in the number of overweight people. According to various authors, between 36.7 and 44 % of asthma patients are obese [2,3]. The results of epidemiological studies show that the presence of obesity almost 2 times increases the chances of asthma developing and, if previously this information was contradictory, now the accumulated data have confirmed this hypothesis [4].…”

“…According to the WHO, the number of patients with asthma in the world is over 330 million people and continues to grow steadily. The disease affects all age groups [1,2].…”