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On the frontier of chronic obstructive pulmonary disease—an interview with Prof. Peter J Barnes
* Corresponding author: Wei Ma, MD
Mailing address: Department of Geriatric Respiratory
Medicine,Guangzhou First People’s Hospital, South China University of Technology, Guangzhou, Guangdong, P.R.510180,
China.
Email: eymawei@scut.edu.cn
Accepted: 20 October 2022 / Published: 29 December 2022
DOI: 10.31491/APT.2022.12.096
Abstract
The article is an interview with Prof. Peter J Barnes of the National Heart and Lung Institute, previously Head of Respiratory Medicine at Imperial College, conducted by Wei Ma of the Department of Geriatric Respiratory Medicine, Guangzhou First People’s Hospital, on behalf of Aging Pathobiology and Therapeutics.
Peter J Barnes, DM, DSc, FRCP, FCCP, FMedSci, FRS
Peter Barnes is Professor of Thoracic Medicine at the
National Heart and Lung Institute, and was Head of Respiratory Medicine at Imperial College and Honorary Consultant Physician at Royal Brompton Hospital, London from
1987-2017.
He qualified at Cambridge and Oxford Universities (first
class honours) He has published over 1500 peer-review
papers on asthma, Chronic Obstructive Pulmonary Disease
(COPD), and related topics (H-index 240) and has written
or edited over 50 books. He is in the top 10 most highly
cited researchers in the world, and has been the most
highly cited respiratory researcher in the world over the
last 30 years.
He was elected a Fellow of the Royal Society in 2007, the
first respiratory researcher for over 150 years. He is a
member of the Scientific Committee of global guidelines
on COPD (GOLD). He also serves on the Editorial Board of
over 30 journals and is currently Editor-in-Chief of Up-to-Date Pulmonary Medicine. He has given several prestigious lectures, including the Amberson Lecture at the American
Thoracic Society, the Sadoul Lecture at the European Respiratory Society, and the Croonian Lecture at the Royal
College of Physicians, London. He has received honorary
degrees from the Universities of Ferrara (Italy), Athens
(Greece), Tampere (Finland), Leuven (Belgium), and Maastricht (Netherlands). He is an NIHR Senior Investigator and
was elected a Master Fellow of the American College of
Chest Physicians and a member of Academia Europaea in
2012. He was President of the European Respiratory Society 2013/2014. He was awarded the Trudeau Medal of
the American Thoracic Society in 2020. He co-founded an
Imperial spin-out company RespiVert, which was acquired
by Johnson & Johnson, and has developed novel inhaled
treatments for COPD and severe asthma.
Wei Ma: Professor Barnes, could you please tell us why
you are interested in the research of COPD and where were
your early passions?
Peter Barnes: I was initially focused on research into asthma, and we worked on the underlying inflammatory mechanisms and the effects of therapies such as corticosteroids
on this inflammation. I then moved on to apply the same
approaches to COPD, as the underlying mechanisms were
much less well understood and there was a greater unmet
need for more effective therapies - even though COPD is
the third-ranked cause of death in the world and a common
cause of hospital admission.
Wei Ma: You have made extraordinary achievements in
your career and you’ve published highly impactful work
in the field of COPD. Can you share your experience in
achieving that?
Peter Barnes: We learned a lot about asthma mechanisms
and treatments using a multidisciplinary approach from
molecular and cell biology through to clinical studies; we
adopted the same approach to investigating COPD. We
were lucky to attract a large team of highly talented clinical and non-clinical scientists to work on the mechanisms of COPD, so were able to produce many publications at
a time when few people were exploring the underlying
mechanisms of the disease.
Wei Ma: Your research is focused on cellular and molecular mechanisms of COPD, what is your latest finding in therapies and biomarkers for COPD?
Peter Barnes: We have been investigating two important
mechanisms in COPD that may be linked. The first is
the role of cellular senescence in driving the pathology,
chronic inflammation, disease progression, and comorbidities in COPD. The second is to understand the cellular
mechanisms of defective phagocytosis of bacteria in COPD
patients that may underlie the bacterial colonization of the
lower airways and may also be linked to cellular senescence.
Wei Ma: You are also involved in multidisciplinary translational research which integrates basic science with clinical studies. Can you provide some novel insights into COPD?
Peter Barnes: I believe that it is very important to link
basic research in cellular and molecular mechanisms to
clinical aspects of COPD, so all of our research is conducted in human cells obtained from carefully phenotyped
COPD patients and appropriate controls. This is important
as animal models of COPD do not closely represent the
human disease.
Wei Ma: What do you think is most valuable to study in
the field of COPD and can you share with us your future
focus?
Peter Barnes: As already mentioned, we are working on
cellular senescence and accelerated ageing of the lung
in COPD, as this may provide a better understanding of
chronic inflammation due to inflammatory mediator release from senescent lung cells, particularly small airway
epithelial cells. We are currently working on how senescence spreads in the lungs through the lungs and beyond
by extracellular vesicles that contain microRNAs that
induce senescence. We think this may account for disease
progression and for comorbidities of COPD which are
usually also diseases of accelerated ageing. Understanding
these mechanisms has identified new therapeutic targets
and biomarkers.
Wei Ma: You are a Senior Research Investigator at the
National Heart and Lung Institute and an Honorary Consultant Physician at Royal Brompton Hospital, and you
have received honorary MD degrees from the Universities
of Ferrara (Italy), Athens (Greece), Tampere (Finland) and
Leuven (Belgium). Can you give some advice for junior
colleagues on how to balance your life and jobs?
Peter Barnes: Research is hard work but very enjoyable
working with an excellent group of colleagues and collaborators. Traveling to scientific meetings around the world
and meeting with others addressing the same research
questions is exciting. However, it is also important to balance work with quality leisure time. I particularly enjoy
traveling with my family and exploring different areas of
the world and often combine this with scientific conferences and meetings.
Wei Ma: How did you decide to get involved with editorial roles? Any advice to help junior faculty/early career researchers on the editorial work?
Peter Barnes: Reviewing manuscripts for journals is a very
valuable way of keeping up to date with the literature, so I
encourage junior colleagues to undertake journal reviews.
I have served on many editorial boards, including acting
as Associate Editor for several journals, which provides an
opportunity to involve more junior researchers in reviewing. I also founded two respiratory journals (Journal of
Pulmonary Pharmacology and Experimental Therapeutics
and Respiratory Research) as there was a need for more
basic research in respiratory medicine.
Wei Ma: Your future focus on lung aging and extracellular vesicles arouses my interest. Extracellular vesicles are
successful in intercellular and interorgan communication
in the aging microenvironment and age-related diseases.
They have detrimental effects on downstream targets at the
levels of immunity, inflammation, gene expression, and
metabolism. What will you choose as downstream targets
of lung aging?
Peter Barnes: We have recently shown that small airway
epithelial cells from COPD patients produce increased
numbers of extracellular vesicles compared to age-matched
controls and that these vesicles are taken up and induce
senescence in normal and COPD epithelial cells via the
transfer of a specific microRNA. We think this is likely to
be an important mechanism for the progression of COPD
and also for many comorbidities through the spread of
these senescence-inducing vesicles via circulation.