Dr Chantal Donovan
Honorary Lecturer
School of Biomedical Sciences and Pharmacy
- Email:chantal.donovan@newcastle.edu.au
- Phone:(02) 4042 0509
Opening up an interest in airways
An undergraduate job in a lab over winter sparked a career focus on lung disease Dr Chantal Donovan’s move to a world-leading respiratory medicine research centre in Newcastle.
Chantal can pinpoint her interest in science as being sparked in high school so she decided to enrol in a Bachelor of Science at the University of Melbourne to help hone her focus. It was while studying pharmacology in her second year, that Chantal found her passion.
Not just content with knowing that drugs worked, Chantal ended up majoring in pharmacology and biochemistry because “I wanted to fully understand how the drugs worked,” Chantal says.
It was during her third year of study that Chantal met a pivotal force in her research: Dr Jane Bourke. “Jane took me on as a winter student and we did a great deal of work into asthma models that really set me on my research path.” Chantal ended up doing honours, and then a PhD with Jane looking at novel therapies for asthma and COPD.
When Jane moved universities, Chantal found a new supervisor, Associate Professor Ross Vlahos who was working with COPD research and smoke models. “I ended up moving what I’d learnt with Jane into Ross’s models and the two ended up combining nicely.”
And this research has continued to inspire Chantal’s work. “We were looking at two different drugs and their impact on airways. The first was rosiglitazone, a drug used for treating type II diabetes which we found actually had an effect relaxing the airways. The second was working with the bitter taste receptors on the tongue. We found that not only are these receptors in the airways, but the drugs that work on them can work to relax the muscle too.
Chantal has already published a substantial body of work, with 18 peer reviewed publications and 25 abstracts as 1st/last author. Her work on understanding the pathogenesis of lung disease, identifying novel targets and therapeutics has been recognised by at the Thoracic Society of Australia and New Zealand and the Australasian Society of Clinical Pharmacologists and Toxicologists society meetings.
A prestigious British Pharmacological Society/ASCEPT Outstanding Young Investigator Award and an array of competitive grants, visiting fellowships and travel awards are testament to Chantal’s standing in the field. Chantal was invited to session chair at the 2016 European Respiratory Society Annual Scientific Meeting in London, and has been a reviewer for a range of journals.
Finding world class facilities in Newcastle
An early career researcher, Chantal has been extremely busy since submitting her PhD in August 2015. The move to Newcastle was considered: Chantal knew she wanted to work with a lung-research lab – so she set about researching the best. And this search led her to the renowned work of Professor Phil Hansbro and his research team. “Of all the labs I’ve looked at in the world, none compares to Phil’s,” Chantal enthuses. “It was quite an easy decision to come here to be honest.”
Before moving from Melbourne, Chantal applied for an NHMRC Early Career Fellowship to work with Phil’s team exploring lung diseases and potential new treatments and preventions. Lung diseases are a major burden on the Australian population and economy. With this work, the team will assess the potential of a new target (IL-33) and therapy (anti-IL-33) in suppressing remodelling in experimental models and human tissues.
Thanks to the success of this application, this work will be a continuation of some of the work that Chantal explored for her PhD “It’s a nice trajectory really,” she adds.
Chantal’s work into IL-33 will explore the role that this protein plays in a number of viral infections and inflammation of the lung. “We know it’s involved, but what’s unknown is how it affects ‘airway remodelling’ which is the scarring of the tissue that you get over time with lung disease.”
“We do know that when you have reduced remodelling you also have reduced IL-33, so what we’re trying to do is understand how and why this happens and whether we can use this information to target the remodelling.”
This work has potential applications for a whole range of lung diseases such as asthma, COPD and IPF. “Remodelling is currently untreated in a whole range of different diseases, so hopefully we can find a link that we can then target.”
Sharing science with parliament
Passionate about raising the profile of science, Chantal attended Science Meets Parliament in Canberra in March 2017. This bi-partisan annual event has been held since 1999 with the aim of urging “all political parties to recognise the importance of science to the nation’s future; economically, socially, culturally and environmentally”.
Chantal was thrilled to have the opportunity to put her respiratory research before the nation’s political leaders. “This event showcases scientific research across all aspects of STEM and provides opportunities to raise issues about the future of research in Australia.”
“By bringing together scientists and politicians, it provides a platform to bridge the gap in knowledge, in particular the needs and concerns of scientists at a government level, with the ultimate goal raising the profile of science in Australia.
“During the meeting I had the honour of meeting the Australian of the Year Emeritus Professor Alan Mackay-Sim and the Honorable Bill Shorten and this two day meeting really provided an eye-opening experience.”
Ensuring that research into lung diseases is effectively funded is a focus on Chantal’s, who acknowledges that science communications and outreach is just another item on a researcher’s to-do list.
Australia has one of the highest rates of lung disease in the world, with one in ten Australians living with a respiratory illness. Chantal’s aim is to help identify gaps in our knowledge which will start to help us identify new therapeutic targets and biomarkers. Watch this space.
Opening up an interest in airways
A job in a lab over winter sparked a career focus on lung disease Dr Chantal Donovan’s move to a world-leading respiratory medicine research centre.
Career Summary
Biography
Dr Donovan is an NHMRC Early Career Post-doctoral Fellow (Peter Doherty Biomedical Fellow) for the Priority Centre for Healthy Lungs and School of Biomedical Science and Pharmacy. She is a member of Professor Phil Hansbro's research team based at the Hunter Medical Research Institute. She completed her PhD (January 2012-April 2015) in the Department of Pharmacology and Therapeutics at the University of Melbourne and Bachelor of Science (Honours) with first class at the University of Melbourne. She completed her first postdoctoral training (April 2015-December 2016) in the Department of Pharmacology at Monash University, with additional training under precision cut lung slice expert Professor Michael Sanderson at the University of Massachusetts Medical School in the USA.
Dr Donovan has 19 peer reviewed publications (13 manuscripts, 6 reviews). She has presented 25 abstracts as 1st/last author and 15 co-author at 13 national & 7 international conferences.
Her research on understanding the pathogenesis of lung disease, identifying novel targets and new therapeutics, is recognised by prestigious oral (x7) and poster (x7) awards at the national respiratory (Thoracic Society of Australia and New Zealand) and pharmacological (Australasian Society of Clinical Pharmacologists and Toxicologist) society meetings. Including the prestigious British Pharmacological Society/ASCEPT Outstanding Young Investigator Award (2016), finalist in the Young Investigator Award (TSANZ, 2014), and the Garth McQueen oral presentation prize for best PhD student (ASCEPT, 2012).
She has obtained over $500k in competitive grants/fellowships, including equipment grants, visiting fellowships, prestigious national (University of Melbourne, UoN) and international (American Thoracic Society, ATS) travel awards, and an international trainee scholarship from the ATS (2016).
Dr Donovan is an expert in a range of mouse models (allergic, bacterial, viral, cigarette smoke) of respiratory disease, assessment of lung function (whole lung mechanics, DLCO, large airway organ bath, small airway myography, precision cut lung slices), and molecular biology (PCR, Western blot, ELISA). She played an integral role in extending the standard outcomes of PCLS in Australia including integrated assessment of molecular signaling pathways and cytokine release.
Qualifications
- Doctor of Philosophy, University of Melbourne
- Bachelor of Science (Honours), University of Melbourne
Keywords
- COPD
- airway remodelling
- asthma
- asthma-COPD overlap
- precision cut lung slices
Publications
For publications that are currently unpublished or in-press, details are shown in italics.
Journal article (59 outputs)
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2024 |
Budden KF, Shukla SD, Bowerman KL, Vaughan A, Gellatly SL, Wood DLA, et al., 'Faecal microbial transfer and complex carbohydrates mediate protection against COPD.', Gut, 73 751-769 (2024) [C1]
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2024 |
Mayall JR, Horvat JC, Mangan NE, Chevalier A, McCarthy H, Hampsey D, et al., 'Interferon-epsilon is a novel regulator of NK cell responses in the uterus', EMBO Molecular Medicine, 16 267-293 [C1]
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2024 |
Gomez HM, Haw TJ, Ilic D, Robinson P, Donovan C, Croft AJ, et al., 'Landscape fire smoke airway exposure impairs respiratory and cardiac function and worsens experimental asthma', Journal of Allergy and Clinical Immunology, (2024)
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2023 |
Donovan C, Bai X, Chan YL, Feng M, Ho KF, Guo H, et al., 'Tenascin C in Lung Diseases', Biology, 12 (2023) [C1] Tenascin C (TNC) is a multifunctional large extracellular matrix protein involved in numerous cellular processes in embryonic development and can be increased in disease, or under... [more] Tenascin C (TNC) is a multifunctional large extracellular matrix protein involved in numerous cellular processes in embryonic development and can be increased in disease, or under conditions of trauma or cell stress in adults. However, the role of TNC in lung diseases remains unclear. In this study, we investigated the expression of TNC during development, in offspring following maternal particulate matter (PM) exposure, asthma, chronic obstructive pulmonary disease (COPD) and lung cancer. TNC expression is increased during lung development in biopsy cells, endothelial cells, mesenchymal cells, and epithelial cells. Maternal PM exposure increased TNC and collagen deposition, which was not affected by the removal of PM exposure after pregnancy. TNC expression was also increased in basal epithelial cells and fibroblasts in patients with asthma and AT2 and endothelial cells in patients with COPD. Furthermore, there was an increase in the expression of TNC in stage II compared to stage IA lung cancer; however, overall survival analysis showed no correlation between levels of TNC and survival. In conclusion, TNC is increased during lung development, in offspring following maternal PM exposure, and in asthma, COPD, and lung cancer tissues. Therefore, targeting TNC may provide a novel therapeutic target for lung diseases.
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2023 |
Tu X, Gomez HM, Kim RY, Brown AC, de Jong E, Galvao I, et al., 'Airway and parenchyma transcriptomics in a house dust mite model of experimental asthma', Respiratory Research, 24 (2023) [C1] Lung transcriptomics studies in asthma have provided valuable information in the whole lung context, however, deciphering the individual contributions of the airway and parenchyma... [more] Lung transcriptomics studies in asthma have provided valuable information in the whole lung context, however, deciphering the individual contributions of the airway and parenchyma in disease pathogenesis may expedite the development of novel targeted treatment strategies. In this study, we performed transcriptomics on the airway and parenchyma using a house dust mite (HDM)-induced model of experimental asthma that replicates key features of the human disease. HDM exposure increased the expression of 3,255 genes, of which 212 were uniquely increased in the airways, 856 uniquely increased in the parenchyma, and 2187 commonly increased in both compartments. Further interrogation of these genes using a combination of network and transcription factor enrichment analyses identified several transcription factors that regulate airway and/or parenchymal gene expression, including transcription factor EC (TFEC), transcription factor PU.1 (SPI1), H2.0-like homeobox (HLX), metal response element binding transcription factor-1 (MTF1) and E74-like factor 4 (ets domain transcription factor, ELF4) involved in controlling innate immune responses. We next assessed the effects of inhibiting lung SPI1 responses using commercially available DB1976 and DB2313 on key disease outcomes. We found that both compounds had no protective effects on airway inflammation, however DB2313 (8¿mg/kg) decreased mucus secreting cell number, and both DB2313 (1¿mg/kg) and DB1976 (2.5¿mg/kg and 1¿mg/kg) reduced small airway collagen deposition. Significantly, both compounds decreased airway hyperresponsiveness. This study demonstrates that SPI1 is important in HDM-induced experimental asthma and that its pharmacological inhibition reduces HDM-induced airway collagen deposition and hyperresponsiveness.
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2023 |
Carroll OR, Pillar AL, Brown AC, Feng M, Chen H, Donovan C, 'Advances in respiratory physiology in mouse models of experimental asthma.', Front Physiol, 14 1099719 (2023) [C1]
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2023 |
Thorpe AE, Donovan C, Kim RY, Vindin HJ, Zakarya R, Miyai H, et al., 'Third-Hand Exposure to E-Cigarette Vapour Induces Pulmonary Effects in Mice', Toxics, 11 (2023) [C1] In the last decade, e-cigarette usage has increased, with an estimated 82 million e-cigarette users globally. This is, in part, due to the common opinion that they are ¿healthier¿... [more] In the last decade, e-cigarette usage has increased, with an estimated 82 million e-cigarette users globally. This is, in part, due to the common opinion that they are ¿healthier¿ than tobacco cigarettes or simply ¿water vapour¿. Third-hand e-vapour exposure is the chemical residue left behind from e-cigarette aerosols, which is of concern due to its invisible nature, especially among young children. However, there is limited information surrounding third-hand e-vapour exposure. This study aimed to investigate the pulmonary effects of sub-chronic third-hand e-vapour exposure in a murine model. BALB/c mice (4 weeks of age) were exposed to a towel containing nicotine free (0 mg) e-vapour, nicotine (18 mg) e-vapour, or no e-vapour (sham) and replaced daily for 4 weeks. At the endpoint, lung function was assessed, and bronchoalveolar lavage fluid and lungs were collected to measure inflammation and fibrosis. Mice exposed to third-hand e-vapour without nicotine had alveolar enlargement compared to sham exposed controls. Mice exposed to third-hand e-vapour with nicotine had reduced bronchial responsiveness to provocation, increased epithelial thickening in large airways, increased epithelial layers in small airways, alveolar enlargement, and increased small airway collagen deposition, compared to sham exposed controls. In conclusion, our study shows that third-hand e-vapour exposure, particularly in the presence of nicotine, negatively affects the lung health of mice and highlights the need for greater public awareness surrounding the dangers of third-hand exposure to e-cigarette vapour.
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2023 |
Van Eeckhoutte HP, Donovan C, Kim RY, Conlon TM, Ansari M, Khan H, et al., 'RIPK1 kinase-dependent inflammation and cell death contribute to the pathogenesis of COPD.', Eur Respir J, 61 (2023) [C1]
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2023 |
Chen H, Burke C, Donovan C, Faiz A, Saad S, Oliver BG, 'E-Cigarette Vapour Alters High-Fat Diet-Induced Systemic Inflammatory Responses but Has No Effect on High-Fat Diet-Induced Changes in Gut Microbiota.', Nutrients, 15 (2023) [C1]
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2023 |
Widjaja M, Kim RY, Donovan C, 'Hybridized face-to-face and online laboratory content in the time of COVID-19.', Biochem Mol Biol Educ, 51 327-328 (2023) [C1]
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2023 |
Horvat JC, Kim RY, Weaver N, Augood C, Brown AC, Donovan C, et al., 'Characterization and inhibition of inflammasome responses in severe and non-severe asthma.', Respir Res, 24 303 (2023) [C1]
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2023 |
Tu J, Li W, Hansbro PM, Yan Q, Bai X, Donovan C, et al., 'Smoking and tetramer tryptase accelerate intervertebral disc degeneration by inducing METTL14-mediated DIXDC1 m6 modification.', Mol Ther, 31 2524-2542 (2023) [C1]
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2023 |
Cooper GE, Mayall J, Donovan C, Haw TJ, Budden KF, Hansbro NG, et al., 'Antiviral Responses of Tissue-resident CD49a+ Lung Natural Killer Cells Are Dysregulated in Chronic Obstructive Pulmonary Disease.', Am J Respir Crit Care Med, 207 553-565 (2023) [C1]
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2023 |
Sahu P, Donovan C, Paudel KR, Pickles S, Chimankar V, Kim RY, et al., 'Pre-clinical lung squamous cell carcinoma mouse models to identify novel biomarkers and therapeutic interventions', FRONTIERS IN ONCOLOGY, 13 (2023) [C1]
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2023 |
Kapellos TS, Baßler K, Fujii W, Nalkurthi C, Schaar AC, Bonaguro L, et al., 'Systemic alterations in neutrophils and their precursors in early-stage chronic obstructive pulmonary disease', Cell Reports, 42 (2023) [C1] Systemic inflammation is established as part of late-stage severe lung disease, but molecular, functional, and phenotypic changes in peripheral immune cells in early disease stage... [more] Systemic inflammation is established as part of late-stage severe lung disease, but molecular, functional, and phenotypic changes in peripheral immune cells in early disease stages remain ill defined. Chronic obstructive pulmonary disease (COPD) is a major respiratory disease characterized by small-airway inflammation, emphysema, and severe breathing difficulties. Using single-cell analyses we demonstrate that blood neutrophils are already increased in early-stage COPD, and changes in molecular and functional neutrophil states correlate with lung function decline. Assessing neutrophils and their bone marrow precursors in a murine cigarette smoke exposure model identified similar molecular changes in blood neutrophils and precursor populations that also occur in the blood and lung. Our study shows that systemic molecular alterations in neutrophils and their precursors are part of early-stage COPD, a finding to be further explored for potential therapeutic targets and biomarkers for early diagnosis and patient stratification.
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2023 |
Lam M, Lamanna E, Organ L, Donovan C, Bourke JE, 'Perspectives on precision cut lung slices powerful tools for investigation of mechanisms and therapeutic targets in lung diseases', Frontiers in Pharmacology, 14 (2023) [C1] Precision cut lung slices (PCLS) have emerged as powerful experimental tools for respiratory research. Pioneering studies using mouse PCLS to visualize intrapulmonary airway contr... [more] Precision cut lung slices (PCLS) have emerged as powerful experimental tools for respiratory research. Pioneering studies using mouse PCLS to visualize intrapulmonary airway contractility have been extended to pulmonary arteries and for assessment of novel bronchodilators and vasodilators as therapeutics. Additional disease-relevant outcomes, including inflammatory, fibrotic, and regenerative responses, are now routinely measured in PCLS from multiple species, including humans. This review provides an overview of established and innovative uses of PCLS as an intermediary between cellular and organ-based studies and focuses on opportunities to increase their application to investigate mechanisms and therapeutic targets to oppose excessive airway contraction and fibrosis in lung diseases.
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2022 |
Pinkerton JW, Kim RY, Brown AC, Rae BE, Donovan C, Mayall JR, et al., 'Relationship between type 2 cytokine and inflammasome responses in obesity-associated asthma', JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 149 1270-1280 (2022) [C1]
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2022 |
Donovan C, Kim RY, Galvao I, Jarnicki AG, Brown AC, Jones-Freeman B, et al., 'Aim2 suppresses cigarette smoke-induced neutrophil recruitment, neutrophil caspase-1 activation and anti-Ly6G-mediated neutrophil depletion', IMMUNOLOGY AND CELL BIOLOGY, 100 235-249 (2022) [C1]
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2022 |
Royce SG, Licciardi PV, Beh RC, Bourke JE, Donovan C, Hung A, et al., 'Sulforaphane prevents and reverses allergic airways disease in mice via anti-inflammatory, antioxidant, and epigenetic mechanisms', CELLULAR AND MOLECULAR LIFE SCIENCES, 79 (2022) [C1]
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2022 |
Tu X, Kim RY, Brown AC, de Jong E, Jones-Freeman B, Ali MK, et al., 'Airway and parenchymal transcriptomics in a novel model of asthma and COPD overlap', Journal of Allergy and Clinical Immunology, 150 817-829.e6 (2022) [C1] Background: Asthma and chronic obstructive pulmonary disease (COPD) are common chronic respiratory diseases, and some patients have overlapping disease features, termed asthma-COP... [more] Background: Asthma and chronic obstructive pulmonary disease (COPD) are common chronic respiratory diseases, and some patients have overlapping disease features, termed asthma-COPD overlap (ACO). Patients characterized with ACO have increased disease severity; however, the mechanisms driving this have not been widely studied. Objectives: This study sought to characterize the phenotypic and transcriptomic features of experimental ACO in mice induced by chronic house dust mite antigen and cigarette smoke exposure. Methods: Female BALB/c mice were chronically exposed to house dust mite antigen for 11 weeks to induce experimental asthma, cigarette smoke for 8 weeks to induce experimental COPD, or both concurrently to induce experimental ACO. Lung inflammation, structural changes, and lung function were assessed. RNA-sequencing was performed on separated airway and parenchyma lung tissues to assess transcriptional changes. Validation of a novel upstream driver SPI1 in experimental ACO was assessed using the pharmacological SPI1 inhibitor, DB2313. Results: Experimental ACO recapitulated features of both asthma and COPD, with mixed pulmonary eosinophilic/neutrophilic inflammation, small airway collagen deposition, and increased airway hyperresponsiveness. Transcriptomic analysis identified common and distinct dysregulated gene clusters in airway and parenchyma samples in experimental asthma, COPD, and ACO. Upstream driver analysis revealed increased expression of the transcription factor Spi1. Pharmacological inhibition of SPI1 using DB2313, reduced airway remodeling and airway hyperresponsiveness in experimental ACO. Conclusions: A new experimental model of ACO featuring chronic dual exposures to house dust mite and cigarette smoke mimics key disease features observed in patients with ACO and revealed novel disease mechanisms, including upregulation of SPI1, that are amenable to therapy.
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2021 |
Tu X, Donovan C, Kim RY, Wark PAB, Horyat JC, Hansbro PM, 'Asthma-COPD overlap: current understanding and the utility of experimental models', EUROPEAN RESPIRATORY REVIEW, 30 (2021) [C1]
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2021 |
Alemao CA, Budden KF, Gomez HM, Rehman SF, Marshall JE, Shukla SD, et al., 'Impact of diet and the bacterial microbiome on the mucous barrier and immune disorders', Allergy: European Journal of Allergy and Clinical Immunology, 76 714-734 (2021) [C1] The prevalence of chronic immune and metabolic disorders is increasing rapidly. In particular, inflammatory bowel diseases, obesity, diabetes, asthma and chronic obstructive pulmo... [more] The prevalence of chronic immune and metabolic disorders is increasing rapidly. In particular, inflammatory bowel diseases, obesity, diabetes, asthma and chronic obstructive pulmonary disease have become major healthcare and economic burdens worldwide. Recent advances in microbiome research have led to significant discoveries of associative links between alterations in the microbiome and health, as well as these chronic supposedly noncommunicable, immune/metabolic disorders. Importantly, the interplay between diet, microbiome and the mucous barrier in these diseases has gained significant attention. Diet modulates the mucous barrier via alterations in gut microbiota, resulting in either disease onset/exacerbation due to a ¿poor¿ diet or protection against disease with a ¿healthy¿ diet. In addition, many mucosa-associated disorders possess a specific gut microbiome fingerprint associated with the composition of the mucous barrier, which is further influenced by host-microbiome and inter-microbial interactions, dietary choices, microbe immigration and antimicrobials. Our review focuses on the interactions of diet (macronutrients and micronutrients), gut microbiota and mucous barriers (gastrointestinal and respiratory tract) and their importance in the onset and/or progression of major immune/metabolic disorders. We also highlight the key mechanisms that could be targeted therapeutically to prevent and/or treat these disorders.
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2021 |
Kim RY, Sunkara KP, Bracke KR, Jarnicki AG, Donovan C, Hsu AC, et al., 'microRNA-21-mediated SATB1/S100A9/NF-kappa B axis promotes chronic obstructive pulmonary disease pathogenesis', SCIENCE TRANSLATIONAL MEDICINE, 13 (2021) [C1]
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2021 |
Gomez HM, Pillar AL, Brown AC, Kim RY, Ali MK, Essilfie A-T, et al., 'Investigating the Links between Lower Iron Status in Pregnancy and Respiratory Disease in Offspring Using Murine Models', NUTRIENTS, 13 (2021) [C1]
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2020 |
Prihandoko R, Kaur D, Wiegman CH, Alvarez-Curto E, Donovan C, Chachi L, et al., 'Pathophysiological regulation of lung function by the free fatty acid receptor FFA4', SCIENCE TRANSLATIONAL MEDICINE, 12 (2020) [C1]
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2020 |
Lo Bello F, Hansbro PM, Donovan C, Coppolino I, Mumby S, Adcock IM, Caramori G, 'New drugs under development for COPD', Expert Opinion on Emerging Drugs, 25 419-431 (2020) [C1] Introduction: Chronic obstructive pulmonary disease (COPD) is a lung disease characterized by chronic bronchitis, emphysema, and remodeling. Its prevalence is increasing worldwide... [more] Introduction: Chronic obstructive pulmonary disease (COPD) is a lung disease characterized by chronic bronchitis, emphysema, and remodeling. Its prevalence is increasing worldwide; however, there are few effective therapies, and none of the treatments currently available prevent the progression of the disease or target all of the hallmark features. The development and progression of COPD are heterogeneous, which has hampered the development of new therapies. Areas covered: In this review, we cover the emergence of the improvement of existing classes of drugs including glucocorticoids, ß2-adrenoceptor agonists, phosphodiesterase inhibitors, PDE4 selective inhibitors, PDE3/PDE4 inhibitors, protease inhibitors, recombinant a1-antitrypsin and neutrophil elastase inhibitors. We also highlight new compounds that target recently identified mechanisms of COPD, new dual-action muscarinic antagonists, and ß2-agonists, kinase inhibitors, cytokine modifiers, chemokines modifiers, NF-¿B inhibitors, senolytics, antioxidants, inhaled antiviral agents, anti-fibrotic compounds, and compounds stimulating lung regeneration. Expert opinion: Given the myriad of potential therapeutic avenues that can be pursued, careful consideration of the phenotypes/endotypes of COPD patients will be important for personalized treatment options in the future, and a full understanding of disease mechanisms in patient subsets will ensure these emerging therapies are targeted appropriately.
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2020 |
Ali MK, Kim RY, Brown AC, Donovan C, Vanka KS, Mayall JR, et al., 'Critical role for iron accumulation in the pathogenesis of fibrotic lung disease', JOURNAL OF PATHOLOGY, 251 49-62 (2020) [C1]
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2020 |
Ali MK, Kim RY, Brown AC, Mayall JR, Karim R, Pinkerton JW, et al., 'Crucial role for lung iron level and regulation in the pathogenesis and severity of asthma', EUROPEAN RESPIRATORY JOURNAL, 55 (2020) [C1]
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2020 |
Johansen MD, Irving A, Montagutelli X, Tate MD, Rudloff I, Nold MF, et al., 'Animal and translational models of SARS-CoV-2 infection and COVID-19', Mucosal Immunology, 13 877-891 (2020) [C1] COVID-19 is causing a major once-in-a-century global pandemic. The scientific and clinical community is in a race to define and develop effective preventions and treatments. The m... [more] COVID-19 is causing a major once-in-a-century global pandemic. The scientific and clinical community is in a race to define and develop effective preventions and treatments. The major features of disease are described but clinical trials have been hampered by competing interests, small scale, lack of defined patient cohorts and defined readouts. What is needed now is head-to-head comparison of existing drugs, testing of safety including in the background of predisposing chronic diseases, and the development of new and targeted preventions and treatments. This is most efficiently achieved using representative animal models of primary infection including in the background of chronic disease with validation of findings in primary human cells and tissues. We explore and discuss the diverse animal, cell and tissue models that are being used and developed and collectively recapitulate many critical aspects of disease manifestation in humans to develop and test new preventions and treatments.
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2020 |
Donovan C, Liu G, Shen S, Marshall JE, Kim RY, Alemao CA, et al., 'The role of the microbiome and the NLRP3 inflammasome in the gut and lung', Journal of Leukocyte Biology, 108 925-935 (2020) [C1] The nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) family, pyrin domain-containing protein 3 (NLRP3) inflammasome, is one of the most well-characterized infla... [more] The nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) family, pyrin domain-containing protein 3 (NLRP3) inflammasome, is one of the most well-characterized inflammasomes, activated by pathogen-associated molecular patterns and damage-associated molecular patterns, including from commensal or pathogenic bacterial and viral infections. The NLRP3 inflammasome promotes inflammatory cell recruitment and regulates immune responses in tissues such as the gastrointestinal tract and the lung, and is involved in many diseases that affect the gut and lung. Recently, the microbiome in the gut and the lung, and the crosstalk between these organs (gut¿lung axis), has been identified as a potential mechanism that may influence disease in a bidirectional manner. In this review, we focus on themes presented in this area at the 2019 World Congress on Inflammation. We discuss recent evidence on how the microbiome can affect NLRP3 inflammasome responses in the gut and lung, the role of this inflammasome in regulating gut and lung inflammation in disease, and its potential role in the gut¿lung axis. We highlight the exponential increase in our understanding of the NLRP3 inflammasome due to the synthesis of the NLRP3 inflammasome inhibitor, MCC950, and propose future studies that may further elucidate the roles of the NLRP3 inflammasome in gut and lung diseases.
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2020 |
Donovan C, Hansbro PM, 'IL-33 in Chronic Respiratory Disease: From Preclinical to Clinical Studies', ACS Pharmacology and Translational Science, 3 56-62 (2020) [C1] IL-33 has been deorphanized as a member of the IL-1 family and has key roles as an alarmin and cytokine with potent capacity to drive type 2 inflammation. This has led to a pletho... [more] IL-33 has been deorphanized as a member of the IL-1 family and has key roles as an alarmin and cytokine with potent capacity to drive type 2 inflammation. This has led to a plethora of studies surrounding its role in chronic diseases with a type 2 inflammatory component. Here, we review the roles of IL-33 in two chronic respiratory diseases, asthma and chronic obstructive pulmonary disease (COPD). We discuss the hallmark and paradigm-shifting studies that have contributed to our understanding of IL-33 biology. We cover animal studies that have elucidated the mechanisms of IL-33 and assessed the role of anti-IL-33 treatment and immunization against IL-33. We highlight key clinical evidence for the potential of targeting increased IL-33 in respiratory diseases including exacerbations, and we outline current clinical trials using an anti-IL-33 monoclonal antibody in asthma patients. Finally, we discuss some of the challenges that have arisen in IL-33 biology and highlight potential future directions in targeting this cytokine in chronic respiratory diseases.
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2019 |
Donovan C, Starkey MR, Kim RY, Rana BMJ, Barlow JL, Jones B, et al., 'Roles for T/B lymphocytes and ILC2s in experimental chronic obstructive pulmonary disease', Journal of Leukocyte Biology, 105 143-150 (2019) [C1] Pulmonary inflammation in chronic obstructive pulmonary disease (COPD) is characterized by both innate and adaptive immune responses; however, their specific roles in the pathogen... [more] Pulmonary inflammation in chronic obstructive pulmonary disease (COPD) is characterized by both innate and adaptive immune responses; however, their specific roles in the pathogenesis of COPD are unclear. Therefore, we investigated the roles of T and B lymphocytes and group 2 innate lymphoid cells (ILC2s) in airway inflammation and remodelling, and lung function in an experimental model of COPD using mice that specifically lack these cells (Rag1 -/- and Rora fl/fl Il7r Cre [ILC2-deficient] mice). Wild-type (WT) C57BL/6 mice, Rag1 -/- , and Rora fl/fl Il7r Cre mice were exposed to cigarette smoke (CS; 12 cigarettes twice a day, 5 days a week) for up to 12¿weeks, and airway inflammation, airway remodelling (collagen deposition and alveolar enlargement), and lung function were assessed. WT, Rag1 -/- , and ILC2-deficient mice exposed to CS had similar levels of airway inflammation and impaired lung function. CS exposure increased small airway collagen deposition in WT mice. Rag1 -/- normal air- and CS-exposed mice had significantly increased collagen deposition compared to similarly exposed WT mice, which was associated with increases in IL-33, IL-13, and ILC2 numbers. CS-exposed Rora fl/fl Il7r Cre mice were protected from emphysema, but had increased IL-33/IL-13 expression and collagen deposition compared to WT CS-exposed mice. T/B lymphocytes and ILC2s play roles in airway collagen deposition/fibrosis, but not inflammation, in experimental COPD.
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2019 |
Caramori G, Ruggeri P, Mumby S, Ieni A, Lo Bello F, Chaminka V, et al., 'Molecular links between COPD and lung cancer: new targets for drug discovery?', Expert Opinion on Therapeutic Targets, 23 539-553 (2019) [C1] Introduction: COPD and lung cancer are leading causes of morbidity and mortality worldwide, and they share a common environmental risk factor in cigarette smoke exposure and a gen... [more] Introduction: COPD and lung cancer are leading causes of morbidity and mortality worldwide, and they share a common environmental risk factor in cigarette smoke exposure and a genetic predisposition represented by their incidence in only a fraction of smokers. This reflects the ability of cigarette smoke to induce an inflammatory response in the airways of susceptible smokers. Moreover, COPD could be a driving factor in lung cancer, by increasing oxidative stress and the resulting DNA damage and repression of the DNA repair mechanisms, chronic exposure to pro-inflammatory cytokines, repression of innate immunity and increased cellular proliferation. Areas covered: We have focused our review on the potential pathogenic molecular links between tobacco smoking-related COPD and lung cancer and the potential molecular targets for new drug development by understanding the common signaling pathways involved in COPD and lung cancer. Expert commentary: Research in this field is mostly limited to animal models or small clinical trials. Large clinical trials are needed but mostly combined models of COPD and lung cancer are necessary to investigate the processes caused by chronic inflammation, including genetic and epigenetic alteration, and the expression of inflammatory mediators that link COPD and lung cancer, to identify new molecular therapeutic targets.
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2019 |
Starkey MR, Plank MW, Casolari P, Papi A, Pavlidis S, Guo Y, et al., 'IL-22 and its receptors are increased in human and experimental COPD and contribute to pathogenesis', EUROPEAN RESPIRATORY JOURNAL, 54 (2019) [C1]
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2018 |
Terlizzi M, Molino A, Colarusso C, Donovan C, Imitazione P, Somma P, et al., 'Activation of the Absent in Melanoma 2 Inflammasome in Peripheral Blood Mononuclear Cells From Idiopathic Pulmonary Fibrosis Patients Leads to the Release of Pro-Fibrotic Mediators', FRONTIERS IN IMMUNOLOGY, 9 (2018) [C1]
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2018 |
Schofield ZV, Croker D, Robertson AAB, Massey NL, Donovan C, Tee E, et al., 'Characterisation of small molecule ligands 4CMTB and 2CTAP as modulators of human FFA2 receptor signalling', SCIENTIFIC REPORTS, 8 (2018) [C1]
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2017 |
Hansbro PM, Kim RY, Starkey MR, Donovan C, Dua K, Mayall JR, et al., 'Mechanisms and treatments for severe, steroid-resistant allergic airway disease and asthma', Immunological Reviews, 278 41-62 (2017) [C1] Severe, steroid-resistant asthma is clinically and economically important since affected individuals do not respond to mainstay corticosteroid treatments for asthma. Patients with... [more] Severe, steroid-resistant asthma is clinically and economically important since affected individuals do not respond to mainstay corticosteroid treatments for asthma. Patients with this disease experience more frequent exacerbations of asthma, are more likely to be hospitalized, and have a poorer quality of life. Effective therapies are urgently required, however, their development has been hampered by a lack of understanding of the pathological processes that underpin disease. A major obstacle to understanding the processes that drive severe, steroid-resistant asthma is that the several endotypes of the disease have been described that are characterized by different inflammatory and immunological phenotypes. This heterogeneity makes pinpointing processes that drive disease difficult in humans. Clinical studies strongly associate specific respiratory infections with severe, steroid-resistant asthma. In this review, we discuss key findings from our studies where we describe the development of representative experimental models to improve our understanding of the links between infection and severe, steroid-resistant forms of this disease. We also discuss their use in elucidating the mechanisms, and their potential for developing effective therapeutic strategies, for severe, steroid-resistant asthma. Finally, we highlight how the immune mechanisms and therapeutic targets we have identified may be applicable to obesity-or pollution-associated asthma.
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2017 |
Jones B, Donovan C, Liu G, Gomez HM, Chimankar V, Harrison CL, et al., 'Animal models of COPD: What do they tell us?', Respirology, 22 21-32 (2017) [C1] COPD is a major cause of global mortality and morbidity but current treatments are poorly effective. This is because the underlying mechanisms that drive the development and progr... [more] COPD is a major cause of global mortality and morbidity but current treatments are poorly effective. This is because the underlying mechanisms that drive the development and progression of COPD are incompletely understood. Animal models of disease provide a valuable, ethically and economically viable experimental platform to examine these mechanisms and identify biomarkers that may be therapeutic targets that would facilitate the development of improved standard of care. Here, we review the different established animal models of COPD and the various aspects of disease pathophysiology that have been successfully recapitulated in these models including chronic lung inflammation, airway remodelling, emphysema and impaired lung function. Furthermore, some of the mechanistic features, and thus biomarkers and therapeutic targets of COPD identified in animal models are outlined. Some of the existing therapies that suppress some disease symptoms that were identified in animal models and are progressing towards therapeutic development have been outlined. Further studies of representative animal models of human COPD have the strong potential to identify new and effective therapeutic approaches for COPD.
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2017 |
Liu G, Cooley MA, Nair PM, Donovan C, Hsu AC, Jarnicki AG, et al., 'Airway remodelling and inflammation in asthma are dependent on the extracellular matrix protein fibulin-1c', JOURNAL OF PATHOLOGY, 243 510-523 (2017) [C1]
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2016 |
Kim RY, Rae B, Neal R, Donovan C, Pinkerton J, Balachandran L, et al., 'Elucidating novel disease mechanisms in severe asthma', CLINICAL & TRANSLATIONAL IMMUNOLOGY, 5 (2016) [C1]
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2016 |
Thorburn AN, Tseng H-Y, Donovan C, Hansbro NG, Jarnicki AG, Foster PS, et al., 'TLR2, TLR4 AND MyD88 Mediate Allergic Airway Disease (AAD) and Streptococcus pneumoniae-Induced Suppression of AAD.', PLoS One, 11 e0156402 (2016) [C1]
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2014 |
Bourke JE, Bai Y, Donovan C, Esposito JG, Tan X, Sanderson MJ, 'Novel small airway bronchodilator responses to rosiglitazone in mouse lung slices', American Journal of Respiratory Cell and Molecular Biology, 50 748-756 (2014) [C1] There is a need to identify novel agents that elicit small airway relaxation when ß2-adrenoceptor agonists become ineffective in difficult-to-treat asthma. Because chronic treatme... [more] There is a need to identify novel agents that elicit small airway relaxation when ß2-adrenoceptor agonists become ineffective in difficult-to-treat asthma. Because chronic treatment with the synthetic peroxisome proliferator activated receptor (PPAR)¿ agonist rosiglitazone (RGZ) inhibits airway hyperresponsiveness in mouse models of allergic airways disease, we tested the hypothesis that RGZ causes acute airway relaxation by measuring changes in small airway size in mouse lung slices. Whereas the ß-adrenoceptor agonists albuterol (ALB) and isoproterenol induced partial airway relaxation, RGZ reversed submaximal and maximal contraction to methacholine (MCh) and was similarly effective after precontraction with serotonin or endothelin-1. Concentration-dependent relaxation to RGZ was not altered by the ß-adrenoceptor antagonist propranolol and was enhanced by ALB. RGZ-induced relaxation wasmimicked by other synthetic PPAR¿ agonists but not by the putative endogenous agonist 15-deoxy-PGJ2 and was not prevented by the PPAR¿ antagonist GW9662. To induce airway relaxation, RGZ inhibited the amplitude and frequency of MCh-induced Ca2+ oscillations of airway smooth muscle cells (ASMCs). In addition, RGZ reduced MCh-induced Ca2+ sensitivity of the ASMCs. Collectively, these findings demonstrate that acute bronchodilator responses induced by RGZ are PPAR¿ independent, additive with ALB, and occur by the inhibition of ASMC Ca2+ signaling and Ca2+ sensitivity. Because RGZ continues to elicit relaxation when ß-adrenoceptor agonists have a limited effect, RGZ or related compounds may have potential as bronchodilators for the treatment of difficult asthma. Copyright © 2014 by the American Thoracic Society.
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2014 |
FitzPatrick M, Donovan C, Bourke JE, 'Prostaglandin E Background: Current asthma therapy may not adequately target contraction of smaller intrapulmonary airways, which are a major site of airway obstruction and inflammation. The aim ... [more] Background: Current asthma therapy may not adequately target contraction of smaller intrapulmonary airways, which are a major site of airway obstruction and inflammation. The aim of this study was to characterise responses of mouse intrapulmonary airways to prostaglandin E2 (PGE2) and compare its dilator efficacy with the ß2-adrenoceptor agonist salbutamol in situ, using lung slices. Methods: Lung slices (150 µm) were prepared from male Balb/C mice. Changes in intrapulmonary airway lumen area were recorded and analysed by phase-contrast microscopy. Relaxation to PGE2 and salbutamol were assessed following various levels of pre-contraction with methacholine, serotonin or endothelin-1, as well as following overnight incubation with PGE2 or salbutamol. The mechanism of PGE2-mediated relaxation was explored using selective EP antagonists (EP1/2 AH6809; EP4 L-161982) and Ca2+-permeabilized slices, where airway responses are due to regulation of Ca2+-sensitivity alone. Results: PGE2 elicited EP1/2-mediated relaxation of intrapulmonary airways. PGE2 was more potent than salbutamol in opposing submaximal pre-contraction to all constrictors tested, and only PGE2 opposed maximal pre-contraction with endothelin-1. Relaxation to PGE2 was maintained when contraction to methacholine was mediated via increased Ca2+-sensitivity alone. PGE2 was less sensitive to homologous or heterologous desensitization of its receptors than salbutamol. Conclusion: The greater efficacy and potency of PGE2 compared to salbutamol in mouse intrapulmonary airways supports further investigation of the mechanisms underlying this improved dilator responsiveness for the treatment of severe asthma. © 2013.
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2014 |
Baker KE, Bonvini SJ, Donovan C, Foong RE, Han B, Jha A, et al., 'Novel drug targets for asthma and COPD: Lessons learned from invitro and invivo models', Pulmonary Pharmacology and Therapeutics, 29 181-198 (2014) [C1] Asthma and chronic obstructive pulmonary disease (COPD) are highly prevalent respiratory diseases characterized by airway inflammation, airway obstruction and airway hyperresponsi... [more] Asthma and chronic obstructive pulmonary disease (COPD) are highly prevalent respiratory diseases characterized by airway inflammation, airway obstruction and airway hyperresponsiveness. Whilst current therapies, such as ß-agonists and glucocorticoids, may be effective at reducing symptoms, they do not reduce disease progression. Thus, there is a need to identify new therapeutic targets. In this review, we summarize the potential of novel targets or tools, including anti-inflammatories, phosphodiesterase inhibitors, kinase inhibitors, transient receptor potential channels, vitamin D and protease inhibitors, for the treatment of asthma and COPD.
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2014 |
Donovan C, Simoons M, Esposito J, Ni Cheong J, FitzPatrick M, Bourke JE, 'Rosiglitazone is a superior bronchodilator compared to chloroquine and ß-adrenoceptor agonists in mouse lung slices', Respiratory Research, 15 (2014) [C1] Background: Current therapy for relieving bronchoconstriction may be ineffective in severe asthma, particularly in the small airways. The aim of this study was to further characte... [more] Background: Current therapy for relieving bronchoconstriction may be ineffective in severe asthma, particularly in the small airways. The aim of this study was to further characterise responses to the recently identified novel bronchodilators rosiglitazone (RGZ) and chloroquine (CQ) under conditions where ß-adrenoceptor agonist efficacy was limited or impaired in mouse small airways within lung slices.Methods: Relaxation to RGZ and CQ was assessed following submaximal methacholine (MCh) pre-contraction, in slices treated overnight with either RGZ, CQ or albuterol (ALB) (to induce ß-adrenoceptor desensitization), and in slices treated with caffeine/ryanodine in which contraction is associated with increases in Ca2+ sensitivity in the absence of contractile agonist-induced Ca2+ oscillations. Furthermore, the effects of RGZ, CQ, ALB and isoproterenol (ISO) on the initiation and development of methacholine-induced contraction were also compared.Results: RGZ and CQ, but not ALB or ISO, elicited complete relaxation with increasing MCh pre-contraction and maintained their potency and efficacy following ß-adrenoceptor desensitization. RGZ, CQ and ALB maintained efficacy following overnight incubation with RGZ or CQ. Relaxation responses to all dilators were generally maintained but delayed after caffeine/ryanodine. Pre-treatment with RGZ, but not CQ, ALB or ISO, reduced MCh potency.Conclusions: This study demonstrates the superior effectiveness of RGZ in comparison to CQ and ß-adrenoceptor agonists as a dilator of mouse small airways. Further investigation of the mechanisms underlying the relatively greater efficacy of RGZ under these conditions are warranted and should be extended to include studies in human asthmatic airways. © 2014 Donovan et al.; licensee BioMed Central Ltd.
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2013 |
Donovan C, Royce SG, Esposito J, Tran J, Ibrahim ZA, Tang MLK, et al., 'Differential Effects of Allergen Challenge on Large and Small Airway Reactivity in Mice', PLoS ONE, 8 (2013) [C1] The relative contributions of large and small airways to hyperresponsiveness in asthma have yet to be fully assessed. This study used a mouse model of chronic allergic airways dis... [more] The relative contributions of large and small airways to hyperresponsiveness in asthma have yet to be fully assessed. This study used a mouse model of chronic allergic airways disease to induce inflammation and remodelling and determine whether in vivo hyperresponsiveness to methacholine is consistent with in vitro reactivity of trachea and small airways. Balb/C mice were sensitised (days 0, 14) and challenged (3 times/week, 6 weeks) with ovalbumin. Airway reactivity was compared with saline-challenged controls in vivo assessing whole lung resistance, and in vitro measuring the force of tracheal contraction and the magnitude/rate of small airway narrowing within lung slices. Increased airway inflammation, epithelial remodelling and fibrosis were evident following allergen challenge. In vivo hyperresponsiveness to methacholine was maintained in isolated trachea. In contrast, methacholine induced slower narrowing, with reduced potency in small airways compared to controls. In vitro incubation with IL-1/TNFa did not alter reactivity. The hyporesponsiveness to methacholine in small airways within lung slices following chronic ovalbumin challenge was unexpected, given hyperresponsiveness to the same agonist both in vivo and in vitro in tracheal preparations. This finding may reflect the altered interactions of small airways with surrounding parenchymal tissue after allergen challenge to oppose airway narrowing and closure. © 2013 Donovan et al.
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Conference (42 outputs)
Year | Citation | Altmetrics | Link | |||||
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2023 |
Mayall J, Pillar A, Daly K, Brown A, Essilfie A-T, Gomez H, et al., 'Iron availability drives influenza A virus infection and associated pathology', RESPIROLOGY (2023)
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2023 |
Mayall J, Pillar A, Daly K, Brown A, Essilfie A-T, Gomez H, et al., 'LSC-2023-Iron metabolism determines the outcome of influenza A virus infection', EUROPEAN RESPIRATORY JOURNAL, IA, Milan (2023)
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2023 |
Mayall J, Cooper G, Donovan C, Haw T, Budden K, Blomme E, et al., 'Anti-viral responses of tissue-resident NK cells are dysregulated in COPD', Christchurch, New Zealand (2023)
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2020 | Bourke JE, Lam M, Allan L, Angeles R, Donovan C, Jaffar J, et al., 'The FFA4 Agonist TUG891 Maintains Bronchodilator Efficacy Under Conditions of Reduced Salbutamol Effectiveness', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, ELECTR NETWORK (2020) | |||||||
2018 | Bourke JE, Angeles R, Donovan C, Royce S, Lam M, 'Free Fatty Acid Receptors 1 and 4 Mediate Desensitisation-Resistant Bronchodilation and Are Expressed in Asthmatic Airways', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, San Diego, CA (2018) | |||||||
2017 | Angeles R, Donovan C, Micallef J, Royce S, Bourke J, 'FREE FATTY ACID RECEPTORS 1 AND 4 ARE NOVEL BRONCHODILATOR TARGETS FOR ASTHMA', RESPIROLOGY (2017) | |||||||
Show 39 more conferences |
Grants and Funding
Summary
Number of grants | 5 |
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Total funding | $650,491 |
Click on a grant title below to expand the full details for that specific grant.
20182 grants / $416,411
Targeting remodelling in chronic obstructive pulmonary disease (COPD), chronic asthma and idiopathic pulmonary fibrosis (IPF)$396,411
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
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Project Team | Doctor Chantal Donovan |
Scheme | Project Grant |
Role | Lead |
Funding Start | 2018 |
Funding Finish | 2020 |
GNo | G1700056 |
Type Of Funding | C1100 - Aust Competitive - NHMRC |
Category | 1100 |
UON | Y |
Investigating the Genetics of the Development of Lung Cancer$20,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
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Project Team | Miss Vrushali Chimankar, Professor Jay Horvat, Doctor Chantal Donovan, Professor Philip Hansbro |
Scheme | Emlyn and Jennie Thomas Postgraduate Medical Research Scholarship |
Role | Investigator |
Funding Start | 2018 |
Funding Finish | 2019 |
GNo | G1800717 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
20173 grants / $234,080
Targeting IL-33 in chronic obstructive pulmonary disease (COPD), chronic asthma and idiopathic pulmonary fibrosis (IPF)$213,007
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
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Project Team | Doctor Chantal Donovan |
Scheme | Early Career Fellowships |
Role | Lead |
Funding Start | 2017 |
Funding Finish | 2020 |
GNo | G1600099 |
Type Of Funding | Aust Competitive - Commonwealth |
Category | 1CS |
UON | Y |
DVCRI Research Support for ECF$11,073
Funding body: University of Newcastle
Funding body | University of Newcastle |
---|---|
Project Team | Doctor Chantal Donovan |
Scheme | NHMRC ECF Support |
Role | Lead |
Funding Start | 2017 |
Funding Finish | 2020 |
GNo | G1700658 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
Flexivent FX base unit controller and software$10,000
Funding body: NSW Ministry of Health
Funding body | NSW Ministry of Health |
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Project Team | Professor Jay Horvat, Doctor Chantal Donovan, Doctor Richard Kim, Doctor Shakti Shukla, Doctor Atiqur Rahman |
Scheme | Medical Research Support Program (MRSP) |
Role | Investigator |
Funding Start | 2017 |
Funding Finish | 2017 |
GNo | G1701220 |
Type Of Funding | C2400 – Aust StateTerritoryLocal – Other |
Category | 2400 |
UON | Y |
Research Supervision
Number of supervisions
Past Supervision
Year | Level of Study | Research Title | Program | Supervisor Type |
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2023 | PhD | Characterisation of the Immune Cell-microbiome Interaction within the Gut-lung Axis in Cigarette Smoke Induced Experimental COPD | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Consultant Supervisor |
2022 | PhD | Understanding the Molecular Mechanisms of Chronic Respiratory Diseases through MultiOmics Approaches | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2022 | PhD | Investigating the Development of New Treatments for Lung Cancer | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2022 | PhD | Investigating New Treatments for Chronic Obstructive Pulmonary Disease | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2022 | PhD | Investigating Asthma-COPD Overlap Using Mouse Models | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2021 | PhD | Investigating the Genetics of the Development of Lung Cancer | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2021 | PhD | Mechanisms and Therapeutic Targeting of Immunometabolism in Lung Disease | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2021 | PhD | Establishing a Murine Model for Early stage Squamous Cell Lung Carcinoma and Understanding the Role of Gut Microbiota in Lung Adenocarcinoma | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
Dr Chantal Donovan
Position
Honorary Lecturer
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing
Contact Details
chantal.donovan@newcastle.edu.au | |
Phone | (02) 4042 0509 |
Link |