Beech Augusta, Higham Andrew, Booth Sophie, Tejwani Vickram, Trinkmann Frederik, Singh Dave
Division of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester and Manchester University NHS Foundation Trust, Manchester, UK.
Medicines Evaluation Unit, Manchester, UK.
Breathe (Sheff). 2024 Nov 12;20(3):230229. doi: 10.1183/20734735.0229-2023. eCollection 2024 Oct.
COPD is a heterogeneous condition, with tobacco smoking being the main environmental risk factor. The presence of type 2 (T2) inflammation is a well-recognised feature of asthma; however, it is now apparent that a subset of COPD patients also displays evidence of T2 inflammation with respect to elevated eosinophil counts and altered gene and protein expression of several T2 inflammatory mediators. T2 inflammatory mediators represent an attractive therapeutic target in both COPD and asthma; however, the efficacy of pharmaceutical interventions varies between diseases. Furthermore, the nature of some shared clinical features also differs. We provide a narrative review of differences in the nature of T2 inflammation between COPD and asthma, which may partly explain phenotypic differences between diseases. We focus on evidence from studies of pulmonary histopathology, sputum and epithelial gene and protein expression, and response to pharmacological interventions targeted at T2 inflammation.
慢性阻塞性肺疾病(COPD)是一种异质性疾病,吸烟是主要的环境风险因素。2型(T2)炎症的存在是哮喘的一个公认特征;然而,现在很明显,一部分COPD患者也表现出T2炎症的证据,表现为嗜酸性粒细胞计数升高以及几种T2炎症介质的基因和蛋白表达改变。T2炎症介质是COPD和哮喘中一个有吸引力的治疗靶点;然而,药物干预的疗效在这两种疾病之间有所不同。此外,一些共同临床特征的性质也有所不同。我们对COPD和哮喘之间T2炎症性质的差异进行了叙述性综述,这可能部分解释了这两种疾病之间的表型差异。我们重点关注来自肺部组织病理学、痰液以及上皮基因和蛋白表达研究的证据,以及针对T2炎症的药物干预反应。