Obesity and Asthma

Abstract

Rationale: Obesity is a major risk factor for asthma; the reasons for this are poorly understood, although it is thought that inflammatory changes in adipose tissue in obesity could contribute to airway inflammation and airway reactivity in individuals who are obese. Objectives: To determine if inflammation in adipose tissue in obesity is related to late-onset asthma, and associated with increased markers of airway inflammation and reactivity. Methods: We recruited a cohort of obese women with asthma and obese control women. We followed subjects with asthma for 12 months after bariatric surgery. We compared markers in adipose tissue and the airway from subjects with asthma and control subjects, and changes in subjects with asthma over time. Measurements and Main Results: Subjects with asthma had increased macrophage infiltration of visceral adipose tissue (P , 0.01), with increased expression of leptin (P , 0.01) and decreased adiponectin (p , 0.001) when controlled for body mass index. Similar trends were observed in subcutaneous adipose tissue. Airway epithelial cells expressed receptors for leptin and adiponectin, and airway reactivity was significantly related to visceral fat leptin expression (rho ¼ 20.8; P , 0.01). Bronchoalveolar lavage cytokines and cytokine production from alveolar macrophages were similar in subjects with asthma and control subjects at baseline, and tended to increase 12 months after surgery. Conclusions: Obesity is associated with increased markers of inflammation in serum and adipose tissue, and yet decreased airway inflammation in obese people with asthma; these patterns reverse with bariatric surgery. Leptin and other adipokines may be important mediators of airway disease in obesity through direct effects on the airway rather than by enhancing airway inflammation.

Endocrine regulation of airway contractility is overlooked

“…The blood level further increases during exacerbation (Tsaroucha et al 2013) and following allergen challenge . Circulating level of leptin also correlates inversely with lung function (Tsaroucha et al 2013) and the expression of leptin in adipose tissue positively correlates with the level of airway responsiveness (Sideleva et al 2012). In agreement with a potentially deleterious effect of leptin in asthma, continuous infusion of leptin by subcutaneously implanted micro-osmotic pumps aggravates AHR in mice sensitized and challenged with an allergen ).…”

Obstructive Sleep Apnea Risk, Asthma Burden, and Lower Airway Inflammation in Adults in the Severe Asthma Research Program (SARP) II

“…Obesity has been suggested to have an important role in promoting the development/severity of asthma. 50 However, obesity is also a well-established risk factor for OSA. 5 Our analyses on associations of OSA symptoms with asthma control measures are adjusted for obesity and suggest a role of OSA in asthma control that is independent of obesity.…”

“…This agrees with recent literature that suggests adipose tissue can directly affect the airway, rather than through enhanced airway inflammation. 50 This phenomenon may explain why studies that addressed the relationship of obesity with lower airway inflammation in asthma have provided negative results, 49, 51 prompting calls to consider OSA in this type of investigations. 29, 49 In addition, interventional studies of CPAP treatment for OSA report improvement in asthma outcomes.…”

Asthma and obesity

“…Данные о со-держании адипонектина при БА и БА, ассоциированной с ожире-нием, противоречивы. Экспрессия AdipoR2 и Т-кадгерина мРНК клетками бронхиального эпителия у мышей с сочетанием БА и ожирения выше, чем у животных либо только с БА, либо только с ожирением [60]. Эксперименты на лабораторных мышах доказа-ли подавляющее действие адипонектина на индуцированную ал-лергенами гиперреактивность дыхательных путей, воспаление дыхательных путей и сократимость гладких мышц бронхиального дерева [61,62].…”