New research led by Edith Cowan University has made an important discovery that could lead to more effective treatments for the world’s 262 million asthma sufferers.
A study led by Dr Stacey Reinke (ECU) and Dr Craig Wheelock (Karolinska Institute, Sweden) found severe asthmatics have a distinct biochemical (metabolite) profile detectable in their urine, compared to mild-to-moderate asthmatics and healthy individuals.
Researchers analysed urine samples from more than 600 participants across 11 countries as part of the U-BIOPRED study, a Europe-wide initiative to identify and better understand different sub-types of severe asthma.
The research team discovered a specific type of metabolite, called carnitines, decreased in severe asthmatics.
Carnitines play an important role in cellular energy generation and immune responses.
Further analyses found carnitine metabolism was lower in severe asthmatics.
These new findings will help enable researchers work towards new, more effective therapies for asthmatics.
A big problem for a lot of people
Dr Reinke, from ECU’s Centre for Integrative Metabolomics and Computational Biology, said it is vital asthma treatment is improved.
“Asthma affects 2.7 million Australians and there were 417 asthma-related deaths in Australia in 2020,” she said.
“Severe asthma occurs when someone’s asthma is uncontrolled, despite being treated with high levels of medication and/or multiple medications.
“To identify and develop new treatment options, we first need to better understand the underlying mechanisms of the disease.”
One way to do this is to examine the body’s chemical profile, or ‘metabolome’, which provides a snapshot of a person’s current physiological state and gives useful insight into disease processes.
“In this case, we were able to use the urinary metabolome of asthmatics to identify fundamental differences in energy metabolism that may represent a target for new interventions in asthma control,” Dr Reinke said.
Can urine really tell us what is happening in the lungs?
Dr Reinke said it can be difficult and invasive to investigate the lungs directly – but fortunately they contain a lot of blood vessels.
“Therefore, any biochemical changes in the lungs can enter the blood stream, and then be excreted through the urine,” she said.
“These are preliminary results, but we will continue to investigate carnitine metabolism to evaluate its potential as a new asthma treatment target.”
‘Urinary metabotype of severe asthma evidences decreased carnitine metabolism independent of oral corticosteroid treatment in the U-BIOPRED study’ was published in the European Respiratory Journal.
European Respiratory Journal
Method of Research
Subject of Research
Urinary metabotype of severe asthma evidences decreased carnitine metabolism independent of oral corticosteroid treatment in the U-BIOPRED study
Article Publication Date
S.N. Reinke reports grants from Canadian Institutes of Health Research, during the conduct of
the study. S. Naz has nothing to disclose. R. Chaleckis has nothing to disclose. H. Gallart-Ayala has nothing to
disclose. J. Kolmert reports personal fees for consultancy from Gesynta Pharma AB, outside the submitted work.
N.Z. Kermani has nothing to disclose. A. Tiotiu has nothing to disclose. D.I. Broadhurst has nothing to disclose.
A. Lundqvist has nothing to disclose. H. Olsson is an employee and shareholder of AstraZeneca. M. Ström has
nothing to disclose. Å.M. Wheelock has nothing to disclose. C. Gómez has nothing to disclose. M. Ericsson has
nothing to disclose. A.R. Sousa has nothing to disclose. J.H. Riley works for and own shares in GlaxoSmithKline.
S. Bates is an employee of Johnson & Johnson and has previously worked for and holds stock in GlaxoSmithKline.
J. Scholfield reports grants from Innovative Medicines Initiative, during the conduct of the study; and is director
and employee of TopMD Precision Medicine Ltd. M. Loza is an employee of and owns stock in Johnson & Johnson.
F. Baribaud is a shareholder of Johnson & Johnson and a current employee of Bristol Myers Squibb. P.S. Bakke
reports personal fees for advisory board work and lectures from AstraZeneca, and personal fees for lectures from
Novartis and Boehringer Ingelheim, outside the submitted work. M. Caruso has nothing to disclose. P. Chanez
reports grants and personal fees from AstraZeneca, ALK, Boehringer Ingelheim, Chiesi, Sanofi-Aventis, Novartis and
GlaxoSmithKline, outside the submitted work. S.J. Fowler reports personal fees from AstraZeneca, Novartis, TEVA
and Chiesi, outside the submitted work. T. Geiser has nothing to disclose. P. Howarth has nothing to disclose.
I. Horvath has nothing to disclose. N. Krug has nothing to disclose. P. Montuschi has nothing to disclose.
A. Behndig has nothing to disclose. F. Singer reports personal fees from Vertex Pharmaceuticals (CH) and Novartis,
outside the submitted work. J. Musial has nothing to disclose. D.E. Shaw has nothing to disclose. B. Dahlén
reports personal fees for advisory board work and lectures from AstraZeneca, TEVA and Sanofi, and grants from
Novartis and GlaxoSmithKline, outside the submitted work. S. Hu has nothing to disclose. J. Lasky-Su has nothing
to disclose. P.J. Sterk reports a public private grant from the Innovative Medicines Initiative (IMI) covered by the
EU and EFPIA, during the conduct of the study. K.F. Chung has received honoraria for participating in advisory
board meetings of GlaxoSmithKline, AstraZeneca, Roche, Novartis, Merck, Nocion and Shionogi regarding
treatments for asthma, COPD and chronic cough and has also been remunerated for speaking engagements.
R. Djukanovic reports receiving fees for lectures at symposia organised by Novartis, AstraZeneca and TEVA,
consultation for TEVA and Novartis as member of advisory boards, and participation in a scientific discussion
about asthma organised by GlaxoSmithKline; and is a co-founder and current consultant, and has shares in
Synairgen, a University of Southampton spin out company. S-E. Dahlén reports personal fees for consultancy from
AstraZeneca, Cayman Chemical, GlaxoSmithKline, Novartis, Merck, Regeneron, Sanofi and TEVA, outside the
submitted work. I.M. Adcock has nothing to disclose. C.E. Wheelock has nothing to disclose.
Support statement: The U-BIOPRED consortium received funding from the European Union and from the European
Federation of Pharmaceutical Industries and Associations as an Innovative Medicines Initiative Joint Undertaking
funded project (number 115010). Grants were also received from the Swedish Heart Lung Foundation, Swedish
Research Council (2016-02798, 2014-3281, 2016-0338), the Konsul Th C Berghs Foundation, the Centre for Allergy
Research Highlights Asthma Markers of Phenotype consortium (funded by the Swedish Foundation for Strategic
Research), the Karolinska Institutet, AstraZeneca and Science for Life Laboratory Joint Research Collaboration, and
the Vårdal Foundation. S.N. Reinke was supported by the Canadian Institutes of Health Research (MFE-135481).
C.E. Wheelock was supported by the Swedish Heart Lung Founda