학술논문
Multiomics links global surfactant dysregulation with airflow obstruction and emphysema in COPD
Document Type
article
Author
Ventzislava A. Hristova; Alastair Watson; Raghothama Chaerkady; Matthew S. Glover; Jodie Ackland; Bastian Angerman; Graham Belfield; Maria G. Belvisi; Hannah Burke; Doriana Cellura; Howard W. Clark; Damla Etal; Anna Freeman; Ashley I. Heinson; Sonja Hess; Michael Hühn; Emily Hall; Alex Mackay; Jens Madsen; Christopher McCrae; Daniel Muthas; Steven Novick; Kristoffer Ostridge; Lisa Öberg; Adam Platt; Anthony D. Postle; C. Mirella Spalluto; Outi Vaarala; Junmin Wang; Karl J. Staples; Tom M.A. Wilkinson; on behalf of the MICA II Study group
Source
ERJ Open Research, Vol 9, Iss 3 (2022)
Subject
Language
English
ISSN
2312-0541
23120541
23120541
Abstract
Rationale Pulmonary surfactant is vital for lung homeostasis as it reduces surface tension to prevent alveolar collapse and provides essential immune-regulatory and antipathogenic functions. Previous studies demonstrated dysregulation of some individual surfactant components in COPD. We investigated relationships between COPD disease measures and dysregulation of surfactant components to gain new insights into potential disease mechanisms. Methods Bronchoalveolar lavage proteome and lipidome were characterised in ex-smoking mild/moderate COPD subjects (n=26) and healthy ex-smoking (n=20) and never-smoking (n=16) controls using mass spectrometry. Serum surfactant protein analysis was performed. Results Total phosphatidylcholine, phosphatidylglycerol, phosphatidylinositol, surfactant protein (SP)-B, SP-A and SP-D concentrations were lower in COPD versus controls (log2 fold change (log2FC) −2.0, −2.2, −1.5, −0.5, −0.7 and −0.5 (adjusted p