Chantal Donovan

ORCID: 0000-0003-4558-329X
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About
Contact & Profiles
Research Areas
  • Asthma and respiratory diseases
  • Chronic Obstructive Pulmonary Disease (COPD) Research
  • IL-33, ST2, and ILC Pathways
  • Neonatal Respiratory Health Research
  • Pediatric health and respiratory diseases
  • Inhalation and Respiratory Drug Delivery
  • Immune Response and Inflammation
  • Respiratory and Cough-Related Research
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • Iron Metabolism and Disorders
  • Inflammasome and immune disorders
  • Air Quality and Health Impacts
  • Peroxisome Proliferator-Activated Receptors
  • Receptor Mechanisms and Signaling
  • Gut microbiota and health
  • Neuroscience of respiration and sleep
  • Pharmacological Effects and Assays
  • Respiratory Support and Mechanisms
  • Eosinophilic Esophagitis
  • Immune Cell Function and Interaction
  • Biochemical Analysis and Sensing Techniques
  • Ion Channels and Receptors
  • Immune cells in cancer
  • S100 Proteins and Annexins
  • Long-Term Effects of COVID-19

Hunter Medical Research Institute
2016-2025

University of Technology Sydney
2019-2025

Woolcock Institute of Medical Research
2022-2025

Macquarie University
2023-2025

Centenary Institute
2019-2024

Immune Regulation (United Kingdom)
2024

University of Newcastle Australia
2020-2024

The University of Sydney
2020-2022

Australian Regenerative Medicine Institute
2015-2018

Monash University
2015-2018

Objective Chronic obstructive pulmonary disease (COPD) is a major cause of global illness and death, most commonly caused by cigarette smoke. The mechanisms pathogenesis remain poorly understood, limiting the development effective therapies. gastrointestinal microbiome has been implicated in chronic lung diseases via gut-lung axis, but its role unclear. Design Using an vivo mouse model smoke (CS)-induced COPD faecal microbial transfer (FMT), we characterised microbiota using metagenomics,...

10.1136/gutjnl-2023-330521 article EN other-oa Gut 2024-02-08

Tobacco smoking is prevalent across the world and causes numerous diseases. Cigarette smoke (CS) compromises immunity, yet little known of components CS that impact T cell function. MR1 a ubiquitous molecule presents bacterial metabolites to MAIT cells, which are highly abundant in lungs. Using silico, cellular, biochemical approaches, we identified bind surface expression. Compounds, including nicotinaldehyde, phenylpropanoid, benzaldehyde-related scaffolds, bound within A′ pocket MR1....

10.1084/jem.20240896 article EN cc-by The Journal of Experimental Medicine 2025-01-17

Five newborn girls presented with small intestinal obstruction and microcolon a giant bladder (megacystis). Organic causes of were not found, the gastrointestinal tract failed to function after appropriate diversion. Two died in postoperative period, two lived several months on central venous hyperalimentation, one at 34 age following chronic though intermittent hyperalimentation. Pathologic studies showed an abundance ganglion cells both dilated narrowed areas intestine; combined...

10.2214/ajr.126.5.957 article EN American Journal of Roentgenology 1976-05-01

Asthma is a chronic inflammatory disease of the airways. It characterized by allergic airway inflammation, remodelling, and hyperresponsiveness (AHR). patients, in particular those with or severe asthma, have remodelling that associated accumulation extracellular matrix (ECM) proteins, such as collagens. Fibulin-1 (Fbln1) an important ECM protein stabilizes collagen other proteins. The level Fbln1c, one four Fbln1 variants, which predominates both humans mice, increased serum airways fluids...

10.1002/path.4979 article EN The Journal of Pathology 2017-09-01

Increased iron levels and dysregulated homeostasis, or both, occur in several lung diseases. Here, the effects of accumulation on pathogenesis pulmonary fibrosis associated function decline was investigated using a combination murine models overload bleomycin-induced fibrosis, primary human fibroblasts treated with iron, histological samples from patients without idiopathic (IPF). Iron are significantly increased overloaded transferrin receptor 2 (Tfr2) mutant mice homeostatic regulator...

10.1002/path.5401 article EN The Journal of Pathology 2020-02-21

Chronic obstructive pulmonary disease (COPD) is the third leading cause of morbidity and death worldwide. Inhalation cigarette smoke (CS) major in developed countries. Current therapies have limited efficacy controlling or halting its progression. Aberrant expression microRNAs (miRNAs) associated with lung disease, including COPD. We performed miRNA microarray analyses lungs mice CS-induced experimental miR-21 was second highest up-regulated miRNA, particularly airway epithelium macrophages....

10.1126/scitranslmed.aav7223 article EN Science Translational Medicine 2021-11-24

Systemic inflammation is established as part of late-stage severe lung disease, but molecular, functional, and phenotypic changes in peripheral immune cells early disease stages remain ill defined. Chronic obstructive pulmonary (COPD) a major respiratory characterized by small-airway inflammation, emphysema, breathing difficulties. Using single-cell analyses we demonstrate that blood neutrophils are already increased early-stage COPD, molecular functional neutrophil states correlate with...

10.1016/j.celrep.2023.112525 article EN cc-by-nc-nd Cell Reports 2023-05-26

We present, here, evidence for a pretranslational role of procollagen propeptides in the regulation collagen synthesis. Amino- and carboxyl-terminal type I were isolated purified from chick calvaria tendon cultures. Human lung fibroblasts (IMR-90) incubated medium containing varying concentrations propeptides. Amino-propeptides at 10 nM caused an 80% decrease synthesis compared to control. Higher amino-propeptides did not further no significant effect on non-collagen was found throughout...

10.1016/s0021-9258(18)67408-3 article EN cc-by Journal of Biological Chemistry 1986-08-01

Chronic obstructive pulmonary disease (COPD) is the third leading cause of morbidity and death globally. The lack effective treatments results from an incomplete understanding underlying mechanisms driving COPD pathogenesis.Interleukin (IL)-22 has been implicated in airway inflammation increased patients. However, its roles pathogenesis poorly understood. Here, we investigated role IL-22 human cigarette smoke (CS)-induced experimental COPD.IL-22 receptor mRNA expression protein levels were...

10.1183/13993003.00174-2018 article EN European Respiratory Journal 2019-06-13

Accumulating evidence highlights links between iron regulation and respiratory disease. Here, we assessed the relationship levels regulatory responses in clinical experimental asthma. We show that cell-free are reduced bronchoalveolar lavage (BAL) supernatant of severe or mild–moderate asthma patients correlate with lower forced expiratory volume 1 s (FEV ). Conversely, iron-loaded cell numbers were increased BAL these FEV /forced vital capacity (FVC) ratio. The airway tissue expression...

10.1183/13993003.01340-2019 article EN European Respiratory Journal 2020-03-17

Background Receptor-interacting protein kinase 1 (RIPK1) is a key mediator of regulated cell death (including apoptosis and necroptosis) inflammation, both drivers COPD pathogenesis. We aimed to define the contribution RIPK1 kinase-dependent inflammation in pathogenesis COPD. Methods assessed expression single-cell RNA sequencing (RNA-seq) data from human mouse lungs, validated levels lung tissue patients via immunohistochemistry. Next, we consequences genetic pharmacological inhibition...

10.1183/13993003.01506-2022 article EN European Respiratory Journal 2022-12-22

Although cigarette smoking (CS) and low back pain (LBP) are common worldwide, their correlations the mechanisms of action remain unclear. We have shown that excessive activation mast cells (MCs) proteases play key roles in CS-associated diseases, like asthma, chronic obstructive pulmonary disease (COPD), blood coagulation, lung cancer. Previous studies also MCs induce degenerative musculoskeletal disease. By using a custom-designed smoke-exposure mouse system, we demonstrated CS results...

10.1016/j.ymthe.2023.06.010 article EN cc-by-nc-nd Molecular Therapy 2023-06-19

Abstract Pulmonary inflammation in chronic obstructive pulmonary disease (COPD) is characterized by both innate and adaptive immune responses; however, their specific roles the pathogenesis of COPD are unclear. Therefore, we investigated T B lymphocytes group 2 lymphoid cells (ILC2s) airway remodelling, lung function an experimental model using mice that specifically lack these (Rag1−/− Rorafl/flIl7rCre [ILC2-deficient] mice). Wild-type (WT) C57BL/6 mice, Rag1−/−, were exposed to cigarette...

10.1002/jlb.3ab0518-178r article EN cc-by Journal of Leukocyte Biology 2018-09-27

Graphical abstractAbstractBackgroundMillions of people are exposed to landscape fire smoke (LFS) globally, and inhalation LFS particulate matter (PM) is associated with poor respiratory cardiovascular outcomes. However, how affects function less well understood.ObjectiveWe aimed characterize the pathophysiologic effects representative airway exposure on cardiac asthma outcomes.MethodsLFS was generated using a customized combustion chamber. In 8-week-old female BALB/c mice, low (25 μg/m3,...

10.1016/j.jaci.2024.02.022 article EN cc-by Journal of Allergy and Clinical Immunology 2024-03-19

The relative contributions of large and small airways to hyperresponsiveness in asthma have yet be fully assessed. This study used a mouse model chronic allergic disease induce inflammation remodelling determine whether vivo methacholine is consistent with vitro reactivity trachea airways. Balb/C mice were sensitised (days 0, 14) challenged (3 times/week, 6 weeks) ovalbumin. Airway was compared saline-challenged controls assessing whole lung resistance, measuring the force tracheal...

10.1371/journal.pone.0074101 article EN cc-by PLoS ONE 2013-09-06
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