The University of Southampton
University of Southampton Institutional Repository

Multiomics links global surfactant dysregulation with airflow obstruction and emphysema in COPD

Multiomics links global surfactant dysregulation with airflow obstruction and emphysema in COPD
Multiomics links global surfactant dysregulation with airflow obstruction and emphysema in COPD
Rationale
Pulmonary surfactant is vital for lung homeostasis as it reduces surface tension to prevent alveolar collapse and provides essential immune-regulatory and anti-pathogenic functions. Previous studies demonstrated dysregulation of some individual surfactant components in COPD.
Objectives
We investigated relationships between COPD disease measures and dysregulation of surfactant components to gain new insights about 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 and surfactant protein (SP)-B, SP-A and SP-D concentrations were lower, COPD vs. controls, log2 fold change (log2FC)=-2.0, -2.2, -1.5, -0.5, -0.7, -0.5 (adj. p-value<0.02), respectively, and correlated with lung function. Total phosphatidylcholine, phosphatidylglycerol, phosphatidylinositol and SP-A, SP-B, SP-D, NAPSA and CD44 inversely correlated with CT small airways disease measures (E/I MLD), r=-0.56, r=-0.58, r=-0.45, r=-0.36, r=-0.44, r=-0.37, r=-0.40, r=-0.39 (adj. p- value<0.05). Total phosphatidylcholine, phosphatidylglycerol, phosphatidylinositol and SP-A, SP-B, SP-D and NAPSA inversely correlated with emphysema (%LAA): r=-0.55, r=-0.61, r=-0.48,
135 r=-0.51, r=-0.41, r=-0.31, r=-0.34, respectively (adj. p-value<0.05). Neutrophil elastase, known to degrade SP-A and SP-D, was elevated, COPD vs. controls, log2FC of 0.40 (adj. p-value=0.0390) and inversely correlated with SP-A and SP-D. Serum SP-D was increased in COPD vs. HV-ES, and predicted COPD status, AUC=0.85.
Conclusions
Using a multiomics approach we, for the first time, demonstrate global surfactant dysregulation in COPD which was associated with emphysema giving new insights about potential mechanisms underlying the cause or consequence of disease.
2312-0541
Hristova, Ventzislava A.
c30fdb39-c86f-4049-aaa9-0a46a9c68844
Watson, Alastair
9eb79329-8d32-4ed4-b8b9-d720883e8042
Chaerkady, Raghothama
848fc1c0-4de4-4494-9365-9b236703807f
Glover, Matthew S.
68d23458-3a4d-4036-8451-4445da52f372
Ackland, Jodie
dba59510-7535-47f8-b2ba-2d49dfa7fbd8
Angermann, Bastian
14d8db65-ad90-4484-b7d8-638b31113058
Belfield, Graham
ad34f8aa-979a-41c6-b011-06dd0936fb39
Belvisi, Maria
5db9e025-50e5-4433-84ae-e19a57402a1e
Burke, Hannah
a9bb9391-4704-4584-aeb7-e69fe0acbdb8
Cellura, Doriana
5edb82b2-f50c-4c76-bd10-8bf687a91b4d
Clark, Howard W.
d237bb0a-ab8f-4b97-8ad2-bbfe73314260
Etal, Damla
641990a2-ac11-435d-9322-b2fe8429439d
Freeman, Anna
b5f45a0d-f9e4-4a91-9af0-40efb6730787
Heinson, Ashley
822775d1-9379-4bde-99c3-3c031c3100fb
Hess, S.
4fb4dd91-1e9d-4da2-9f13-ac68089d1fd8
Hühn, Michael
5229e389-760b-47a5-9ffa-cdb6430719b5
Hall, Emily
3b4f235a-2cca-43a8-b4a8-c2d6a8791201
Mackay, Alex
05ea4c2a-4829-4396-b861-ab4cbcc15033
Madsen, Jens
b5d8ae35-00ac-4d19-930e-d8ddec497359
McCrae, Christopher
905349d4-6151-412b-b146-7f1481d8472b
Muthas, Daniel
6928e069-9767-4a26-85f6-b5407073612d
Novick, Steven
b101de8a-1ef2-475c-9f9c-13de38b036a0
Ostridge, Kristoffer
d2271bae-b078-4390-8919-8f8c0e20542c
Oberg, Lisa
1da2b5af-dfdc-493e-acc1-30f7b5dcf10b
Platt, Adam
1cf7f1f0-5b57-407d-b6f1-51b5bebc204d
Postle, Anthony
0fa17988-b4a0-4cdc-819a-9ae15c5dad66
Spalluto, Cosma Mirella
6802ad50-bc38-404f-9a19-40916425183b
Vaarala, Outi
35ea8119-e804-402c-bb79-cfac625e71f5
Wang, Junmin
4ba25ffb-6ede-4cfd-befd-40e9e2c212b4
Staples, Karl J.
e0e9d80f-0aed-435f-bd75-0c8818491fee
Wilkinson, Tom MA
8c55ebbb-e547-445c-95a1-c8bed02dd652
MICA II Studygroup
Hristova, Ventzislava A.
c30fdb39-c86f-4049-aaa9-0a46a9c68844
Watson, Alastair
9eb79329-8d32-4ed4-b8b9-d720883e8042
Chaerkady, Raghothama
848fc1c0-4de4-4494-9365-9b236703807f
Glover, Matthew S.
68d23458-3a4d-4036-8451-4445da52f372
Ackland, Jodie
dba59510-7535-47f8-b2ba-2d49dfa7fbd8
Angermann, Bastian
14d8db65-ad90-4484-b7d8-638b31113058
Belfield, Graham
ad34f8aa-979a-41c6-b011-06dd0936fb39
Belvisi, Maria
5db9e025-50e5-4433-84ae-e19a57402a1e
Burke, Hannah
a9bb9391-4704-4584-aeb7-e69fe0acbdb8
Cellura, Doriana
5edb82b2-f50c-4c76-bd10-8bf687a91b4d
Clark, Howard W.
d237bb0a-ab8f-4b97-8ad2-bbfe73314260
Etal, Damla
641990a2-ac11-435d-9322-b2fe8429439d
Freeman, Anna
b5f45a0d-f9e4-4a91-9af0-40efb6730787
Heinson, Ashley
822775d1-9379-4bde-99c3-3c031c3100fb
Hess, S.
4fb4dd91-1e9d-4da2-9f13-ac68089d1fd8
Hühn, Michael
5229e389-760b-47a5-9ffa-cdb6430719b5
Hall, Emily
3b4f235a-2cca-43a8-b4a8-c2d6a8791201
Mackay, Alex
05ea4c2a-4829-4396-b861-ab4cbcc15033
Madsen, Jens
b5d8ae35-00ac-4d19-930e-d8ddec497359
McCrae, Christopher
905349d4-6151-412b-b146-7f1481d8472b
Muthas, Daniel
6928e069-9767-4a26-85f6-b5407073612d
Novick, Steven
b101de8a-1ef2-475c-9f9c-13de38b036a0
Ostridge, Kristoffer
d2271bae-b078-4390-8919-8f8c0e20542c
Oberg, Lisa
1da2b5af-dfdc-493e-acc1-30f7b5dcf10b
Platt, Adam
1cf7f1f0-5b57-407d-b6f1-51b5bebc204d
Postle, Anthony
0fa17988-b4a0-4cdc-819a-9ae15c5dad66
Spalluto, Cosma Mirella
6802ad50-bc38-404f-9a19-40916425183b
Vaarala, Outi
35ea8119-e804-402c-bb79-cfac625e71f5
Wang, Junmin
4ba25ffb-6ede-4cfd-befd-40e9e2c212b4
Staples, Karl J.
e0e9d80f-0aed-435f-bd75-0c8818491fee
Wilkinson, Tom MA
8c55ebbb-e547-445c-95a1-c8bed02dd652

Hristova, Ventzislava A., Watson, Alastair, Chaerkady, Raghothama, Glover, Matthew S., Ackland, Jodie, Angermann, Bastian, Belfield, Graham, Belvisi, Maria, Burke, Hannah, Cellura, Doriana, Clark, Howard W., Etal, Damla, Freeman, Anna, Heinson, Ashley, Hess, S., Hühn, Michael, Hall, Emily, Mackay, Alex, Madsen, Jens, McCrae, Christopher, Muthas, Daniel, Novick, Steven, Ostridge, Kristoffer, Oberg, Lisa, Platt, Adam, Postle, Anthony, Spalluto, Cosma Mirella, Vaarala, Outi, Wang, Junmin, Staples, Karl J. and Wilkinson, Tom MA , MICA II Studygroup (2022) Multiomics links global surfactant dysregulation with airflow obstruction and emphysema in COPD. ERJ Open Research. (In Press)

Record type: Article

Abstract

Rationale
Pulmonary surfactant is vital for lung homeostasis as it reduces surface tension to prevent alveolar collapse and provides essential immune-regulatory and anti-pathogenic functions. Previous studies demonstrated dysregulation of some individual surfactant components in COPD.
Objectives
We investigated relationships between COPD disease measures and dysregulation of surfactant components to gain new insights about 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 and surfactant protein (SP)-B, SP-A and SP-D concentrations were lower, COPD vs. controls, log2 fold change (log2FC)=-2.0, -2.2, -1.5, -0.5, -0.7, -0.5 (adj. p-value<0.02), respectively, and correlated with lung function. Total phosphatidylcholine, phosphatidylglycerol, phosphatidylinositol and SP-A, SP-B, SP-D, NAPSA and CD44 inversely correlated with CT small airways disease measures (E/I MLD), r=-0.56, r=-0.58, r=-0.45, r=-0.36, r=-0.44, r=-0.37, r=-0.40, r=-0.39 (adj. p- value<0.05). Total phosphatidylcholine, phosphatidylglycerol, phosphatidylinositol and SP-A, SP-B, SP-D and NAPSA inversely correlated with emphysema (%LAA): r=-0.55, r=-0.61, r=-0.48,
135 r=-0.51, r=-0.41, r=-0.31, r=-0.34, respectively (adj. p-value<0.05). Neutrophil elastase, known to degrade SP-A and SP-D, was elevated, COPD vs. controls, log2FC of 0.40 (adj. p-value=0.0390) and inversely correlated with SP-A and SP-D. Serum SP-D was increased in COPD vs. HV-ES, and predicted COPD status, AUC=0.85.
Conclusions
Using a multiomics approach we, for the first time, demonstrate global surfactant dysregulation in COPD which was associated with emphysema giving new insights about potential mechanisms underlying the cause or consequence of disease.

Text
ERJOR-00378-2022.R1_Proof_hi Submitted 21st Sept - Accepted Manuscript
Restricted to Repository staff only
Request a copy

More information

Accepted/In Press date: 16 October 2022

Identifiers

Local EPrints ID: 471595
URI: http://eprints.soton.ac.uk/id/eprint/471595
ISSN: 2312-0541
PURE UUID: 48971889-d1ce-4f88-b1d5-9117296a88fa
ORCID for Jodie Ackland: ORCID iD orcid.org/0000-0003-3120-3620
ORCID for Hannah Burke: ORCID iD orcid.org/0000-0003-3553-4590
ORCID for Anna Freeman: ORCID iD orcid.org/0000-0003-3495-2520
ORCID for Ashley Heinson: ORCID iD orcid.org/0000-0001-8695-6203
ORCID for Jens Madsen: ORCID iD orcid.org/0000-0003-1664-7645
ORCID for Anthony Postle: ORCID iD orcid.org/0000-0001-7361-0756
ORCID for Cosma Mirella Spalluto: ORCID iD orcid.org/0000-0001-7273-0844
ORCID for Karl J. Staples: ORCID iD orcid.org/0000-0003-3844-6457

Catalogue record

Date deposited: 14 Nov 2022 17:50
Last modified: 17 Mar 2024 04:07

Export record

Contributors

Author: Ventzislava A. Hristova
Author: Alastair Watson
Author: Raghothama Chaerkady
Author: Matthew S. Glover
Author: Jodie Ackland ORCID iD
Author: Bastian Angermann
Author: Graham Belfield
Author: Maria Belvisi
Author: Hannah Burke ORCID iD
Author: Doriana Cellura
Author: Howard W. Clark
Author: Damla Etal
Author: Anna Freeman ORCID iD
Author: Ashley Heinson ORCID iD
Author: S. Hess
Author: Michael Hühn
Author: Emily Hall
Author: Alex Mackay
Author: Jens Madsen ORCID iD
Author: Christopher McCrae
Author: Daniel Muthas
Author: Steven Novick
Author: Kristoffer Ostridge
Author: Lisa Oberg
Author: Adam Platt
Author: Anthony Postle ORCID iD
Author: Cosma Mirella Spalluto ORCID iD
Author: Outi Vaarala
Author: Junmin Wang
Author: Karl J. Staples ORCID iD
Corporate Author: MICA II Studygroup

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of http://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×