Obesity and asthma: Possible mechanisms

ArticleinThe Journal of allergy and clinical immunology 121(5):1087-93; quiz 1094-5 · June 2008with15 Reads
DOI: 10.1016/j.jaci.2008.03.004 · Source: PubMed
Abstract
Epidemiologic data indicate that obesity increases the prevalence and incidence of asthma and reduces asthma control. Obese mice exhibit innate airway hyperresponsiveness and augmented responses to certain asthma triggers, further supporting a relationship between obesity and asthma. Here I discuss several mechanisms that may explain this relationship. In obesity, lung volume and tidal volume are reduced, events that promote airway narrowing. Obesity also leads to a state of low-grade systemic inflammation that may act on the lung to exacerbate asthma. Obesity-related changes in adipose-derived hormones, including leptin and adiponectin, may participate in these events. Comorbidities of obesity, such as dyslipidemia, gastroesophageal reflux, sleep-disordered breathing, type 2 diabetes, or hypertension may provoke or worsen asthma. Finally, obesity and asthma may share a common etiology, such as common genetics, common in utero conditions, or common predisposing dietary factors. Novel therapeutic strategies for treatment of the obese patient with asthma may result from an increased understanding of the mechanisms underlying this relationship.
    • "An exacerbation of asthma may lead to long hospitalization and death. Asthma can be exacerbated by several risk factors such as type two diabetes mellitus (T2-DM), obesity or high body mass index (BMI), hypertension, gastroesophageal reflux and sleep-disorder breathing [3]. However, the presence of clustering conditions such as, metabolic syndrome has strong association with asthma [4, 5]. "
    [Show abstract] [Hide abstract] ABSTRACT: Asthma is a major burden on global health care system which is encumbering all regions in the world. Several risk factors can induce and exacerbate asthma. Recent compelling evidences have associated metabolic syndrome with the incidence of asthma. The abdominal obesity, hypertension and insulin resistance are metabolic syndrome criteria which are substantially involved in inducing and exacerbating asthma. Several mechanisms are involved in the association between metabolic syndrome and asthma. It could be due to mechanical reason, genetic factors, inflammatory effect, hormonal effect, insulin resistance and the effect of other co-morbidities associated with obesity. In this review, we discuss the mechanisms which link metabolic syndrome to asthma.
    Article · Aug 2016 · Postgraduate Medicine
    • "This finding is consistent with others finding no relationship between increased inflammation and depressed lung function associated with ozone exposure in healthy normal subjects [10, 30] . Future chamber studies might consider targeting obese and normal weight individuals with asthma, i.e. those with both a greater baseline airway reactivity/inflammation and response to ozone [1, 3]. The combined effect of exercise and ozone exposure appeared to enhance the baseline difference in systemic inflammation between the obese and normal weight individuals. "
    [Show abstract] [Hide abstract] ABSTRACT: We previously observed greater ozone-induced lung function decrements in obese than non-obese women. Animal models suggest that obesity enhances ozone-induced airway reactivity and inflammation. In a controlled exposure study, we compared the acute effect of randomized 0.4ppm ozone and air exposures (2 h with intermittent light exercise) in obese (N = 20) (30<BMI<40Kg/m2) vs. non-obese (N = 20) (BMI<25Kg/m2) non-smoking 18–35 year old women. We measured spirometry and bronchial reactivity to inhaled methacholine (3h post-exposure). Inflammation and obesity markers were assessed in the blood (pre, 4h post, and 20h post exposures) and induced-sputum (4h post-exposures and on 24h pre-exposure training day, no exercise): measures of C reactive protein (CRP) (blood only), leptin (blood only), adiponectin, interleukins IL-6, IL-1b, and IL-8, and tumor necrosis factor alpha, and sputum cell differential cell counts. The pre- to post-exposure decrease in forced vital capacity after ozone (adjusted for the change after air exposure) was significantly greater in the obese group (12.5+/-7.5 vs. 8.0+/-5.8%, p<0.05). Post ozone exposure, 6 obese and 6 non-obese subjects responded to methacholine at ≤ 10mg/ml (the maximum dose); the degree of hyperresponsiveness was similar for the two groups. Both BMI groups showed similar and significant ozone-induced increases in sputum neutrophils. Plasma IL-6 was increased by exercise (4 hr post air exposure vs. pre) only in the obese but returned to pre-air exposure levels at 20hr post-exposure. Plasma IL-6 was significantly increased at 4hr post ozone exposure in both groups and returned to pre-exposure levels by 20h post-exposure. These results confirm our previous findings of greater post-ozone spirometric decrements in obese young women. However, acute ozone-induced airway reactivity to methacholine and airway inflammation did not differ by obesity at the exposure and exercise levels used.
    Full-text · Article · Aug 2016
    • "Several mechanisms have been proposed by which obesity could be associated to exacerbations of asthma, including the production of pro-inflammatory cytokines and chemokines (i.e. eotaxin, leptin, IL-6 and TNF-a) [37]. Interestingly, and besides the fact that our patients who experienced exacerbations had increased biomarkers related to eosinophilic inflammation, no single biomarker was related to exacerbations in the multivariate Poisson regression analysis. "
    [Show abstract] [Hide abstract] ABSTRACT: Objectives: Although modern treatment of asthma improves asthma control, some patients still experience exacerbations. The aim of the present study was to detect predictors of asthmatic exacerbations Methods: We included patients with asthma followed up in asthma clinics of 2 tertiary University hospitals. Demographic and functional characteristics, levels of exhaled NO, and inflammatory biomarkers (IL-13, ΕCP και IL-8) and cell counts in induced sputum were recorded at baseline. Measurements were performed with the patients in stability and were considered as their personal best. Patients received optimal treatment with good compliance and were followed up for 1 year for asthma exacerbations occurrence. Evaluation of the effect of recorded parameters on asthma exacerbations was performed with univariate and multivariate Poisson regression analysis. Results: 171 patients (118 female) with bronchial asthma (mean age 51.6±13.2 years) were included in the study. The mean number of exacerbations in 1 year of follow up was 0.4±0.8 while the majority of patients (71.9%) did not experience any exacerbation. In multivariate Poisson Regression analysis only 3 characteristics were predictors of future exacerbations: FEV1 [IRR(95% CI)], [0.970(0.954-0.987)], p=0.001, high BMI [1.078(1.030-1.129)], p=0.001, and the need for permanent treatment with oral corticosteroids for asthma control maintenance [2.542(1.083-5.964)], p=0.032 Conclusion: Optimal guideline-based asthma management results in minimal occurrence of exacerbations in the majority of patients. Predictors of exacerbations are low FEV1 levels in stability, high BMI and the need for permanent treatment with oral corticosteroids.
    Full-text · Article · Aug 2016
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