ERJ Open Research (Feb 2024)

Aberrant characteristics of peripheral blood innate lymphoid cells in COPD, independent of smoking history

  • Cathelijne M. van Zelst,
  • Johannes C.C.M. in ’t Veen,
  • Lisette Krabbendam,
  • Geertje M. de Boer,
  • Marjolein J.W. de Bruijn,
  • Menno van Nimwegen,
  • Esmee K. van der Ploeg,
  • Denise van Uden,
  • Ralph Stadhouders,
  • Gerdien A. Tramper-Stranders,
  • Rudi W. Hendriks,
  • Gert-Jan Braunstahl

DOI
https://doi.org/10.1183/23120541.00652-2023
Journal volume & issue
Vol. 10, no. 1

Abstract

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Background Distinguishing asthma and COPD can pose challenges in clinical practice. Increased group 1 innate lymphoid cells (ILC1s) have been found in the lungs and peripheral blood of COPD patients, while asthma is associated with elevated levels of ILC2s. However, it is unclear whether the inflammatory characteristics of ILC1s and ILC2s differ between COPD and asthma. This study aims to compare peripheral blood ILC subsets and their expression of inflammatory markers in COPD patients, asthma patients and controls. Methods The study utilised multi-colour flow cytometry to analyse peripheral blood ILC populations in clinically stable COPD patients (n=38), asthma patients (n=37), and smoking (n=19) and non-smoking (n=16) controls. Results Proportions of peripheral blood inflammatory CD4+ ILC1s were significantly higher in COPD patients than in asthma. Proportions of CD4− ILC1s were increased in COPD patients compared to asthma patients and smoking controls. Frequencies of CD117− ILC2s were significantly reduced in COPD patients compared with asthma patients. In contrast, the fraction of inflammatory CD45RO+ cells within the CD117− ILC2 population was significantly increased. Principal component analyses showed that combined features of the circulating ILC compartment separated COPD patients from asthma patients and both control groups. Conclusion Our in-depth characterisation of ILC1 and ILC2 populations in peripheral blood revealed significant differences in their phenotypes between COPD and asthma patients and smoking or non-smoking controls. These findings suggest a role for both ILC subsets in COPD disease pathology, independent of smoking history, and may have implications for patient stratification and therapy development.