한빛사논문
- 조회233
Firoozeh V. Gerayeli1,9, Hye Yun Park1,2,9, Stephen Milne1,3, Xuan Li1, Chen Xi Yang1, Josie Tuong1,4, Rachel L Eddy1,5, Seyed Milad Vahedi1,4, Elizabeth Guinto1, Chung Y Cheung1, Julia SW Yang1, Cassie Gilchrist1, Dina Yehia1, Tara Stach6, Hong Dang7, Clarus Leung1,5, Tawimas Shaipanich5, Jonathon Leipsic8, Graeme J. Koelwyn1,4, Janice M. Leung1,5 and Don D. Sin1,5⇑
1Centre for Heart Lung Innovation, St. Paul's Hospital, Vancouver, BC, Canada
2Division of Pulmonary and Critical Care Medicine, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea
3Faculty of Medicine & Health, University of Sydney, Sydney, NSW, Australia
4Faculty of Health Sciences, Simon Fraser University, Burnaby, Canada
5Division of Respiratory Medicine, Department of Medicine, University of British Columbia, Vancouver, BC, Canada
6Biomedical Research Centre, School of Biomedical Engineering, UBC, Vancouver, BC, Canada
7University of North Carolina Chapel Hill, Cystic Fibrosis and Pulmonary Disease Research and Treatment Center, Chapel Hill, USA
8Department of Radiology, University of British Columbia, Vancouver, Canada
9Firoozeh V. Gerayeli and Hye Yun Park contributed equally as co-first authors
⇑Corresponding author: Don D. Sin
Abstract
To elucidate the important cellular and molecular drivers of pulmonary long COVID, we generated a single-cell transcriptomic map of the airway mucosa using bronchial brushings from patients with long COVID who reported persistent pulmonary symptoms.
Adults with and without long COVID were recruited from the general community in Greater Vancouver, Canada. The cohort was divided into those with pulmonary long COVID (PLC), which was defined as persons with new or worsening respiratory symptoms following at least one year from their initial acute SARS-CoV-2 infection (N=9); and control subjects defined as SARS-CoV-2 infected persons whose acute respiratory symptoms had fully resolved or individuals who had no history of acute COVID-19 (N=9). These participants underwent bronchoscopy from which a single cell suspension was created from bronchial brush samples and then sequenced.
A total of 56 906 cells were recovered for the downstream analysis, with 34 840 cells belonging to the PLC group, which strikingly showed a unique cluster of neutrophils in the PLC group (p<0.05). Ingenuity Pathway Analysis revealed that the neutrophil degranulation pathway was enriched across epithelial cell clusters. Differential gene expression analysis between the PLC and control groups demonstrated upregulation of inflammatory chemokines and epithelial barrier dysfunction across epithelial cell clusters, as well as over-expression of mucin genes across secretory cell clusters.
In conclusion, a single-cell transcriptomic landscape of the small airways suggest that neutrophils may play a significant role in mediating the chronic small airway inflammation driving pulmonary symptoms of long COVID.
논문정보
- Research article
- 2024년 09월 (BRIC 등록일 2024-09-30)
- 국내+국외 연구진
- 의약학 > 응용의학
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