Department of Respiratory and Critical Care Medicine, Singapore General Hospital, Singapore, Singapore.
Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore.
Eur Respir J. 2024 Nov 28;64(5). doi: 10.1183/13993003.00907-2024. Print 2024 Nov.
Sensitisation to is linked to worse outcomes in patients with COPD; however, its prevalence and clinical implications in domestic (residential) settings remains unknown.
Individuals with COPD (n=43) recruited in Singapore had their residences prospectively sampled and assessed by shotgun metagenomic sequencing including indoor air, outdoor air and touch surfaces (a total of 126 specimens). The abundance of environmental and the occurrence of (Asp f) allergens in the environment were determined and immunological responses to allergens determined in association with clinical outcomes including exacerbation frequency. Findings were validated in 12 individuals (31 specimens) with COPD in Vancouver, Canada, a climatically different region.
157 metagenomes from 43 homes were assessed. 11 and nine separate spp were identified in Singapore and Vancouver, respectively. Despite climatic, temperature and humidity variation, was detectable in the environment from both locations. The relative abundance of environmental was significantly associated with exacerbation frequency in both Singapore (r=0.27, p=0.003) and Vancouver (r=0.49, p=0.01) and individuals with higher Asp f 3 sensitisation responses lived in homes with a greater abundance of environmental Asp f 3 allergens (p=0.037). Patients exposed and sensitised to Asp f 3 allergens demonstrated a higher rate of COPD exacerbations at 1-year follow-up (p=0.021).
Environmental exposure in the home environment including air and surfaces with resulting sensitisation carries pathogenic potential in individuals with COPD. Targeting domestic abundance may reduce COPD exacerbations.
在 COPD 患者中，对 的致敏与更差的结局相关；然而，其在国内（住宅）环境中的流行率和临床意义尚不清楚。
在新加坡招募的 COPD 患者（n=43）的住宅进行前瞻性采样，并通过 shotgun 宏基因组测序进行评估，包括室内空气、室外空气和接触表面（共 126 个标本）。确定环境中 的丰度和环境中 的 （Asp f）过敏原的发生，并确定与临床结局（包括加重频率）相关的免疫反应。在加拿大温哥华的 12 名 COPD 患者（31 个标本）中验证了这些发现，温哥华的气候条件不同。
评估了来自 43 个家庭的 157 个宏基因组。在新加坡和温哥华分别鉴定出 11 种和 9 种单独的 spp。尽管气候、温度和湿度存在差异，但仍可在两个地点的环境中检测到 。环境中 的相对丰度与新加坡（r=0.27，p=0.003）和温哥华（r=0.49，p=0.01）的加重频率显著相关，并且具有更高的 Asp f 3 致敏反应的个体生活在环境中具有更高丰度的环境 Asp f 3 过敏原的家庭中（p=0.037）。在 1 年随访时，暴露于 Asp f 3 过敏原并致敏的患者 COPD 加重的发生率更高（p=0.021）。
住宅环境中包括空气和表面在内的 暴露以及由此产生的致敏在 COPD 患者中具有致病潜力。靶向家庭内 的丰度可能会减少 COPD 加重。
