Editors' ChoiceAsthma

Asthma super-sized

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Science Translational Medicine  11 Nov 2015:
Vol. 7, Issue 313, pp. 313ec192
DOI: 10.1126/scitranslmed.aad5508

Obesity is a known risk factor for asthma. Indeed, obese individuals with asthma have a harder time controlling their asthma, and inhaled steroids do not work as well in obese persons as in lean individuals. Yet the mechanistic connection between these two seemingly unrelated conditions remains unclear. One hypothesis is that the proinflammatory state induced by obesity may contribute to the airway inflammation in asthmatics. Here, Diaz et al. used a mouse model of house dust mite–induced asthma to examine the effects of obesity on markers of inflammation and immunity and response to glucocorticoid treatment. Plasma adiponectin, an anti-inflammatory cytokine produced by adipocytes and proposed to be protective against asthma, was lower in obese compared with lean mice. However, plasma immunoglobulin E (IgE) levels, an indicator of allergen hyperresponsiveness, were increased in obese mice. Moreover, in lung tissues, eosinophil counts were lower; yet macrophage counts were higher in obese mice, suggesting that obesity shifts the quality of immune cell infiltrates. These data were supported by higher amounts of macrophage marker mRNA expression in lung tissue and enhanced macrophage infiltration of bronchoalveolar lavage fluid of obese mice. These differences may affect the response to therapeutics. Treating obese mice with the glucocorticoid dexamethasone failed to improve some measures of inflammation and macrophage infiltration in obese mice. Taken together, this study implicates macrophage infiltration as a distinct phenotype of obese asthmatic lungs and as a possible mechanism for reduced sensitivity to inhaled steroids in obesity. Additional studies examining the immune cell profiles of obese and lean patients with asthma are needed.

J. Diaz et al., Obesity shifts house dust mite–induced airway cellular infiltration from eosinophils to macrophages: Effects of glucocorticoid treatment. Immunol. Res. 10.1007/s12026-015-8717-2 (2015). [Abstract]

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