Kim Sang-Ha, Sutherland E Rand, Gelfand Erwin W
Department of Pediatrics, National Jewish Health, Denver, Colorado, USA. ; Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea.
Department of Medicine, National Jewish Health, Denver, Colorado, USA.
Allergy Asthma Immunol Res. 2014 May;6(3):189-95. doi: 10.4168/aair.2014.6.3.189. Epub 2014 Mar 7.
Increasing epidemiological data identify a link between obesity and asthma incidence and severity. Based on experimental data, it is possible that shared inflammatory mechanisms play a role in determining this linkage. Although controversial, the role of adipokines may be central to this association and the maintenance of the asthma phenotype. While leptin and adiponectin have a causal link to experimental asthma in mice, data in humans are less conclusive. Recent studies demonstrate that adipokines can regulate the survival and function of eosinophils and that these factors can affect eosinophil trafficking from the bone marrow to the airways. In addition, efferocytosis, the clearance of dead cells, by airway macrophages or blood monocytes appears impaired in obese asthmatics and is inversely correlated with glucocorticoid responsiveness. This review examines the potential mechanisms linking obesity to asthma.
越来越多的流行病学数据表明肥胖与哮喘的发病率及严重程度之间存在联系。基于实验数据,共享的炎症机制可能在决定这种联系中发挥作用。尽管存在争议,但脂肪因子的作用可能是这种关联以及哮喘表型维持的核心。虽然瘦素和脂联素与小鼠实验性哮喘存在因果联系,但人类的数据尚无定论。最近的研究表明,脂肪因子可调节嗜酸性粒细胞的存活和功能,并且这些因素可影响嗜酸性粒细胞从骨髓向气道的转运。此外,肥胖哮喘患者气道巨噬细胞或血液单核细胞的胞葬作用(即清除死细胞)似乎受损,且与糖皮质激素反应性呈负相关。本综述探讨了将肥胖与哮喘联系起来的潜在机制。