Exploring Type 2 Inflammation in Chronic Obstructive Pulmonary Disease

Deborah Liao
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Abstract

This symposium took place during the 2023 meeting of the European Respiratory Society (ERS), with a focus on targeting chronic obstructive pulmonary disease (COPD) with Type 2 inflammation, and the emerging biologic landscape. The speakers discussed the clinical consequences of COPD through an understanding of pathological changes, the spectrum of inflammatory pathways, the role of Type 2 inflammation in the pathophysiology of COPD, and the evolving clinical landscape in COPD. Klaus Rabe, Full Member (Chair), LungenClinic, Grosshansdorf, Germany, utilised hypothetical clinical scenarios to contextualise the clinical presentation of COPD as a consequence of disease pathology, specifically chronic inflammation leading to structural changes of airways and parenchymal destruction resulting in airflow limitation, leading to worsening symptoms, and increasing further exacerbation risk. Stephanie Christenson, Assistant Professor of pulmonology at the University of California, San Francisco, USA, followed with a discussion of the heterogeneity of inflammatory pathways, exploration of distinct inflammatory cells and cytokines, and the evolving state of the knowledge of the diverse inflammatory pathways associated with COPD. COPD inflammation can be differentiated by distinct inflammatory cells and cytokines into Type 1/Type 3 inflammation (i.e., neutrophilic inflammation) and Type 2 inflammation. However, there is potential overlap in the various inflammatory mechanisms driving COPD via the alarmins IL-33 and thymic stromal lymphopoietin. In addition, the key cytokines IL-4, IL-13, and IL-5 mediate the pathophysiology of COPD with Type 2 inflammation. Altogether, the heterogeneous inflammatory pathways contribute to characteristic features of COPD, fibrosis (small airways), wall thickening, airway remodelling, and clinical features, such as shortness of breath at rest. Dave Singh, Professor of respiratory pharmacology at The University of Manchester, UK, then discussed active areas of investigation in the development of additional treatments for patients with COPD.
慢性阻塞性肺疾病2型炎症的探讨
本次研讨会在2023年欧洲呼吸学会(ERS)会议期间举行,重点关注慢性阻塞性肺疾病(COPD)伴2型炎症和新兴生物学景观。演讲者通过对病理变化、炎症途径谱、2型炎症在慢性阻塞性肺病病理生理中的作用以及慢性阻塞性肺病临床前景的理解,讨论了慢性阻塞性肺病的临床后果。Klaus Rabe,德国格罗斯山斯多夫LungenClinic的正式成员(主席),利用假设的临床情景,将慢性阻塞性肺病的临床表现作为疾病病理的结果,特别是慢性炎症导致气道结构改变和实质破坏,导致气流限制,导致症状恶化,并增加进一步恶化的风险。Stephanie Christenson,美国加州大学旧金山分校肺脏学助理教授,随后讨论了炎症途径的异质性,探索不同的炎症细胞和细胞因子,以及与COPD相关的多种炎症途径的知识发展状况。COPD炎症可通过不同的炎症细胞和细胞因子分化为1/ 3型炎症(即嗜中性粒细胞炎症)和2型炎症。然而,通过警报因子IL-33和胸腺基质淋巴生成素驱动COPD的各种炎症机制存在潜在的重叠。此外,关键细胞因子IL-4、IL-13、IL-5介导COPD伴2型炎症的病理生理。总之,异质性炎症途径导致COPD的特征性特征,纤维化(小气道)、壁增厚、气道重塑和临床特征,如静息时呼吸短促。英国曼彻斯特大学呼吸药理学教授Dave Singh随后讨论了针对慢性阻塞性肺病患者开发其他治疗方法的活跃研究领域。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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