Firestone Institute for Respiratory Health, St Joseph's Healthcare & Department of Medicine, McMaster University, 50 Charlton Avenue East, Hamilton, ON, L8N 4A6, Canada.
Respir Res. 2018 Feb 27;19(1):33. doi: 10.1186/s12931-018-0741-z.
Asthma and obesity, two growing epidemics worldwide, may share an underlying causal relationship. Airway hyperresponsiveness (AHR), a defining component of asthma, has been documented in both 'obese' animal models and non-asthmatic obese individuals. However, there is a paucity of evidence that obesity-derived factors directly affect human airway smooth muscles (ASM).
Experiments were designed with primary ASM and adipocytes isolated from the same human tissue explants (n = 6). The modulatory effects of human adipocytes extracted from subcutaneous (extrathoracic) and visceral (intrathoracic) depots, on ASM biology was examined with respect to proliferation, migration, contractility and pro-inflammatory cytokine synthesis.
Adipocyte-conditioned media as well as myocyte-adipocyte co-cultures failed to show any significant changes in the proliferative or migrational properties of the ASM. Adipocyte-conditioned media also had no effect on the contractility or relaxation of bovine tracheal muscle strips. In contrast, there was a moderate yet significant increase of IL-6 and eotaxin release by ASM incubated with adipocyte-conditioned media (P = 0.0035 and P = 0.0067, vs. control, respectively), thereby further consolidating the altered inflammatory state reported for both diseases.
We report, for the first time, that adipocytes from either subcutaneous or visceral depots can trigger an inflammatory state in the ASM, with negligible modulatory effects on hyperplasia, hypertrophy or contractile properties.
哮喘和肥胖症是全球范围内两个不断增长的流行疾病，它们可能存在潜在的因果关系。气道高反应性（AHR）是哮喘的一个定义性特征，已在“肥胖”动物模型和非哮喘肥胖个体中得到证实。然而，肥胖相关因素直接影响人类气道平滑肌（ASM）的证据很少。
从相同的人体组织外植体中分离出原代 ASM 和脂肪细胞，设计了实验（n=6）。研究了从皮下（胸外）和内脏（胸内）脂肪组织中提取的人类脂肪细胞对 ASM 生物学的调节作用，包括增殖、迁移、收缩和促炎细胞因子合成。
脂肪细胞条件培养基以及肌细胞-脂肪细胞共培养均未显示 ASM 增殖或迁移特性的任何显著变化。脂肪细胞条件培养基对牛气管平滑肌条的收缩和松弛也没有影响。相比之下，与对照相比，用脂肪细胞条件培养基孵育的 ASM 释放出中等但显著增加的 IL-6 和嗜酸性粒细胞趋化因子（P=0.0035 和 P=0.0067），从而进一步证实了这两种疾病的改变的炎症状态。
我们首次报道，来自皮下或内脏脂肪组织的脂肪细胞可以引发 ASM 的炎症状态，对增生、肥大或收缩特性几乎没有调节作用。
