Abstract
BackgroundA clear relationship between asthma and obesity has been reported, but the mechanisms remain unclear. The aim of this study was to evaluate the influence of obesity on eosinophil activity (chemotaxis and adhesion) in asthmatic children and adolescents compared with cells from healthy volunteers.MethodsAsthmatic obese (AO), asthmatic non-obese (ANO), non-asthmatic obese (NAO) and non-asthmatic non-obese (NANO) individuals were included in the present study. The chemotaxis of eosinophils after stimulation with eotaxin (300 ng/ml), platelet-activating factor (10 μM; PAF) and RANTES (100 ng/ml) was performed using a microchemotaxis chamber. The eosinophil peroxidase activity was measured to determine the adhesion activity of eosinophils cultivated on fibronectin-coated plates. The serum leptin, adiponectin, TNF-α and IgE levels were quantified using ELISA assays.ResultsThe serum IgE levels and eosinophil counts were significantly higher in asthmatic (obese and non-obese) individuals compared with non-asthmatic individuals (obese and non-obese). Spontaneous eosinophil chemotaxis was greater in the AO group compared with either the ANO or NANO groups. The activation of eosinophils using eotaxin and PAF increased eosinophil chemotaxis in the AO group. RANTES treatment increased eosinophil chemotaxis in the NAO group compared with the NANO or ANO groups. The activation of eosinophils using eotaxin significantly increased eosinophil adhesion in the AO group compared with other groups. The serum leptin and TNF-α levels were higher in obese subjects (asthmatic and non-asthmatic), whereas the levels of adiponectin did not significantly differ among these groups.ConclusionThis study is the first to show increased eosinophilic activity (chemotaxis and adhesion) associated with high serum leptin and TNF-α levels in atopic asthmatic obese children and adolescents compared with non-obese healthy volunteers.
Highlights
A clear relationship between asthma and obesity has been reported, but the mechanisms remain unclear
To the best of our knowledge, there are no studies concerning in vitro eosinophilic activities in asthmatic obese individuals
The asthma diagnosis was established according to the criteria of the American Thoracic Society-European Respiratory Society (ATS-ERS) [27], and the degree of asthma was classified according to the Global Initiative for Asthma (GINA) as intermittent, mild persistent, moderate persistent and severe persistent asthma [28]
Summary
A clear relationship between asthma and obesity has been reported, but the mechanisms remain unclear. The aim of this study was to evaluate the influence of obesity on eosinophil activity (chemotaxis and adhesion) in asthmatic children and adolescents compared with cells from healthy volunteers. In murine models of dietinduced obesity and allergic diseases, ovalbumin challenge promotes hyperresponsiveness and eosinophilic inflammation associated with increased lung Th2 cytokines, serum IgE and lung parenchyma remodelling [23,24,25]. To the best of our knowledge, there are no studies concerning in vitro eosinophilic activities (chemotaxis and adhesion) in asthmatic obese individuals. We hypothesised that the increase in obesity-associated systemic inflammatory mediators activates eosinophils, thereby exacerbating pulmonary inflammation, which is a direct component of asthma pathophysiology. The aim of this study was to evaluate the influence of obesity on peripheral blood eosinophil functions (chemotaxis and adhesion) in asthmatic children and adolescents
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