Dr Su Ling Loo
Postdoctoral Research Fellow
School of Biomedical Sciences and Pharmacy
- Email:suling.loo@newcastle.edu.au
- Phone:(02) 40420107
Career Summary
Biography
Qualifications
- Doctor of Philosophy, University of Newcastle
- Bachelor of Science, University of Newcastle
- Bachelor of Biomedical Sciences (Hons), University of Newcastle
Keywords
- bronchial epithelial cells
- cell culture
- coronavirus
- rhinovirus
- virus infection
Fields of Research
Code | Description | Percentage |
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310706 | Virology | 60 |
320103 | Respiratory diseases | 40 |
Professional Experience
UON Appointment
Title | Organisation / Department |
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Postdoctoral Research Fellow | University of Newcastle School of Biomedical Sciences and Pharmacy Australia |
Awards
Prize
Year | Award |
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2018 |
Best Presentation in the Cell, Immunology and Molecular Biology of the Lung SIG The Thoracic Society of Australia & New Zealand |
2017 |
Translational Basic Science Award PRC For Healthy Lungs, University of Newcastle |
2017 |
Lung Foundation Australia sponsored David Serisier Memorial Award for Translational Research (Respiratory Infectious Disease) SIG Award The Thoracic Society of Australia and New Zealand |
Publications
For publications that are currently unpublished or in-press, details are shown in italics.
Chapter (3 outputs)
Year | Citation | Altmetrics | Link | ||||||||
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2019 |
Esneau C, Croft S, Loo SL, Ghildyal R, 'Rhinovirus diversity and virulence factors', Rhinovirus Infections: Rethinking the Impact on Human Health and Disease 25-59 (2019) The rhinovirus (RV) genus is highly diverse, consisting of three species and more than 167 subtypes, utilizing three different receptors for cell entry. This diversity has been an... [more] The rhinovirus (RV) genus is highly diverse, consisting of three species and more than 167 subtypes, utilizing three different receptors for cell entry. This diversity has been an obstacle to the development of effective cross-reactive antiviral treatments or vaccine strategies. Accumulating research suggests a possible association of virus species/subtypes with illness severity presenting the possibility for antiviral approaches targeting specific subtypes instead of all RVs. To facilitate such an approach, identification of the underlying molecular mechanism and the viral factor/s that mediate disease is required. Recent literature shows a clear species/subtype associated divergence in the host cell directed activity of RV proteases. Whether these differences correlate with the subtype-specific differences in illness severity remains to be confirmed. In this chapter, we bring together current knowledge of the association of RV species/subtypes with illness and explore the possible role of RV proteases as the main virulence factors associated with illness severity.
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2019 |
Reid AT, Sutanto EN, Chander-Veerati P, Looi K, Li NF, Iosifidis T, et al., 'Ground zero-the airway epithelium', Rhinovirus Infections: Rethinking the Impact on Human Health and Disease, Academic Press, Cambridge, MS 61-98 (2019) [B1]
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2014 |
Hsu ACY, Loo SL, Fathi Aghdam F, Parsons K, Hansbro PM, Wark PAB, 'Airway Epithelial and Early Innate Immune Responses to Virus Infections', Human Respiratory Viral Infections 29-44 (2014) This introduction presents an overview of the key concepts discussed in the subsequent chapters of this book. The book describes respiratory viruses are important human pathogens ... [more] This introduction presents an overview of the key concepts discussed in the subsequent chapters of this book. The book describes respiratory viruses are important human pathogens due to their propensity to cause disease and their fast transmission rate among humans via aerosols. They are the most common cause of infection and frequently lead to a large burden of illness and increased mortality, as well as high socioeconomic cost. The consequence of respiratory viral infections is clearly dependent upon complex interactions between the host and pathogen. The importance of any shift in these interactions is illustrated by the enhanced susceptibility of those with chronic respiratory disease to infection. Viral respiratory tract infections remain an important medical and social problem, ranging from trivial infections to life-threatening episodes. As knowledge in regard to the innate immune response in the airways has increased, it is becoming increasingly recognized that this early response is crucial in determining the outcome of virus infection.
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Journal article (8 outputs)
Year | Citation | Altmetrics | Link | ||||||||
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2022 |
Williams TC, Loo S-L, Nichol KS, Reid AT, Veerati PC, Esneau C, et al., 'IL-25 blockade augments antiviral immunity during respiratory virus infection', COMMUNICATIONS BIOLOGY, 5 (2022) [C1]
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2021 |
Girkin J, Loo S-L, Esneau C, Maltby S, Mercuri F, Chua B, et al., 'TLR2-mediated innate immune priming boosts lung anti-viral immunity', EUROPEAN RESPIRATORY JOURNAL, 58 (2021) [C1]
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2021 |
Williams TC, Jackson DJ, Maltby S, Walton RP, Ching Y-M, Glanville N, et al., 'Rhinovirus-induced CCL17 and CCL22 in Asthma Exacerbations and Differential Regulation by STAT6', AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 64 344-356 (2021) [C1]
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2021 |
Finney LJ, Glanville N, Farne H, Aniscenko J, Fenwick P, Kemp SV, et al., 'Inhaled corticosteroids downregulate the SARS-CoV-2 receptor ACE2 in COPD through suppression of type I interferon', Journal of Allergy and Clinical Immunology, 147 510-519.e5 (2021) [C1] Background: The mechanisms underlying altered susceptibility and propensity to severe Coronavirus disease 2019 (COVID-19) disease in at-risk groups such as patients with chronic o... [more] Background: The mechanisms underlying altered susceptibility and propensity to severe Coronavirus disease 2019 (COVID-19) disease in at-risk groups such as patients with chronic obstructive pulmonary disease (COPD) are poorly understood. Inhaled corticosteroids (ICSs) are widely used in COPD, but the extent to which these therapies protect or expose patients to risk of severe COVID-19 is unknown. Objective: The aim of this study was to evaluate the effect of ICSs following pulmonary expression of the SARS-CoV-2 viral entry receptor angiotensin-converting enzyme-2 (ACE2). Methods: We evaluated the effect of ICS administration on pulmonary ACE2 expression in vitro in human airway epithelial cell cultures and in vivo in mouse models of ICS administration. Mice deficient in the type I IFN-a/ß receptor (Ifnar1-/-) and administration of exogenous IFN-ß were used to study the functional role of type-I interferon signaling in ACE2 expression. We compared sputum ACE2 expression in patients with COPD stratified according to use or nonuse of ICS. Results: ICS administration attenuated ACE2 expression in mice, an effect that was reversed by exogenous IFN-ß administration, and Ifnar1-/- mice had reduced ACE2 expression, indicating that type I interferon contributes mechanistically to this effect. ICS administration attenuated expression of ACE2 in airway epithelial cell cultures from patients with COPD and in mice with elastase-induced COPD-like changes. Compared with ICS nonusers, patients with COPD who were taking ICSs also had reduced sputum expression of ACE2. Conclusion: ICS therapies in COPD reduce expression of the SARS-CoV-2 entry receptor ACE2. This effect may thus contribute to altered susceptibility to COVID-19 in patients with COPD.
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2020 |
Loo SL, Wark PAB, Esneau C, Nichol KS, Hsu ACY, Bartlett NW, 'Human coronaviruses 229E and OC43 replicate and induce distinct antiviral responses in differentiated primary human bronchial epithelial cells', American Journal of Physiology - Lung Cellular and Molecular Physiology, 319 L926-L931 (2020) [C1] The recurrent emergence of novel, pathogenic coronaviruses (CoVs) severe acute respiratory syndrome coronavirus 1 (SARS-CoV-1; 2002), Middle East respiratory syndrome (MERS)-CoV (... [more] The recurrent emergence of novel, pathogenic coronaviruses (CoVs) severe acute respiratory syndrome coronavirus 1 (SARS-CoV-1; 2002), Middle East respiratory syndrome (MERS)-CoV (2012), and most recently SARS-CoV-2 (2019) has highlighted the need for physiologically informative airway epithelial cell infection models for studying immunity to CoVs and development of antiviral therapies. To address this, we developed an in vitro infection model for two human coronaviruses; alphacoronavirus 229E-CoV (229E) and betacoronavirus OC43-CoV (OC43) in differentiated primary human bronchial epithelial cells (pBECs). Primary BECs from healthy subjects were grown at air-liquid interface (ALI) and infected with 229E or OC43, and replication kinetics and time-course expression of innate immune mediators were assessed. OC43 and 229E-CoVs replicated in differentiated pBECs but displayed distinct replication kinetics: 229E replicated rapidly with viral load peaking at 24 h postinfection, while OC43 replication was slower peaking at 96 h after infection. This was associated with diverse antiviral response profiles defined by increased expression of type I/III interferons and interferon-stimulated genes (ISGs) by 229E compared with no innate immune activation with OC43 infection. Understanding the host-virus interaction for previously established coronaviruses will give insight into pathogenic mechanisms underpinning SARS-CoV-2-induced respiratory disease and other future coronaviruses that may arise from zoonotic sources.
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2019 |
Singanayagam A, Loo SL, Calderazzo M, Finney LJ, Torralbo MBT, Bakhsoliani E, et al., 'Antiviral immunity is impaired in COPD patients with frequent exacerbations', American Journal of Physiology - Lung Cellular and Molecular Physiology, 317 L893-L903 (2019) [C1] Patients with frequent exacerbations represent a chronic obstructive pulmonary disease (COPD) subgroup requiring better treatment options. The aim of this study was to determine t... [more] Patients with frequent exacerbations represent a chronic obstructive pulmonary disease (COPD) subgroup requiring better treatment options. The aim of this study was to determine the innate immune mechanisms that underlie susceptibility to frequent exacerbations in COPD. We measured sputum expression of immune mediators and bacterial loads in samples from patients with COPD at stable state and during virusassociated exacerbations. In vitro immune responses to rhinovirus infection in differentiated primary bronchial epithelial cells (BECs) sampled from patients with COPD were additionally evaluated. Patients were stratified as frequent exacerbators (=2 exacerbations in the preceding year) or infrequent exacerbators (<2 exacerbations in the preceding year) with comparisons made between these groups. Frequent exacerbators had reduced sputum cell mRNA expression of the antiviral immune mediators type I and III interferons and reduced interferon-stimulated gene (ISG) expression when clinically stable and during virus-associated exacerbation. A role for epithelial cellintrinsic innate immune dysregulation was identified: induction of interferons and ISGs during in vitro rhinovirus (RV) infection was also impaired in differentiated BECs from frequent exacerbators. Frequent exacerbators additionally had increased sputum bacterial loads at 2 wk following virus-associated exacerbation onset. These data implicate deficient airway innate immunity involving epithelial cells in the increased propensity to exacerbations observed in some patients with COPD. Therapeutic approaches to boost innate antimicrobial immunity in the lung could be a viable strategy for prevention and treatment of frequent exacerbations.
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2018 |
Singanayagam A, Glanville N, Girkin JL, Ching YM, Marcellini A, Porter JD, et al., 'Corticosteroid suppression of antiviral immunity increases bacterial loads and mucus production in COPD exacerbations', NATURE COMMUNICATIONS, 9 (2018) [C1]
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2016 |
Loo S-L, Wark PAB, 'Recent advances in understanding and managing asthma.', F1000Res, 5 (2016) [C1]
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Show 5 more journal articles |
Conference (7 outputs)
Year | Citation | Altmetrics | Link | ||
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2022 |
Bartlett NW, Williams T, Loo S, Girkin J, 'IL-25 Inhibits Airway Anti-Viral Immunity and Promotes Virus Exacerbation of Allergic Airways Disease', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, San Francisco, CA (2022)
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2022 |
Anderson GP, Jarnicki A, Loo S, Ciccotosto J, Girkin J, O'Donoghue R, et al., 'Development of TLR2/6 Agonist (INNA-051) to Protect the Elderly Against Respiratory Virus Infection', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, CA, San Francisco (2022)
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2022 |
Girkin J, Bryant NE, Loo S, Demaison C, Mercuri F, Bartlett NW, 'TLR2/6 Agonist Treatment Enhances Antiviral Innate Immune Responses in a Novel Mouse Coronavirus Respiratory Infection Model', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, San Francisco, CA (2022)
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2015 |
Loo S, Hsu A, Hansbro P, Wark P, 'THE ROLE OF PI3 KINASE IN INFLUENZA H1N1 AND RHINOVIRUS VIRAL ENTRY INTO PRIMARY BRONCHIAL EPITHELIAL CELLS', RESPIROLOGY, Queensland, AUSTRALIA (2015) [E3]
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Show 4 more conferences |
Preprint (1 outputs)
Year | Citation | Altmetrics | Link | |||||
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2019 |
Singanayagam A, Loo S-L, Calderazzo M, Finney L, Trujillo Torralbo M-B, Bakhsoliani E, et al., 'Anti-microbial immunity is impaired in COPD patients with frequent exacerbations (2019)
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Grants and Funding
Summary
Number of grants | 2 |
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Total funding | $100,261 |
Click on a grant title below to expand the full details for that specific grant.
20192 grants / $100,261
Define the mechanism of action and determine the efficacy of the Company’s therapeutic drug$50,261
Funding body: Ena Therapeutics Pty Ltd
Funding body | Ena Therapeutics Pty Ltd |
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Project Team | Professor Nathan Bartlett, Doctor Su Ling Loo |
Scheme | Entrepreneurs' Programme: Innovation Connections |
Role | Investigator |
Funding Start | 2019 |
Funding Finish | 2019 |
GNo | G1900110 |
Type Of Funding | C3100 – Aust For Profit |
Category | 3100 |
UON | Y |
Define the mechanism of action and determine the efficacy of the Company’s therapeutic drug$50,000
Funding body: Department of Industry, Innovation and Science
Funding body | Department of Industry, Innovation and Science |
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Project Team | Professor Nathan Bartlett, Doctor Su Ling Loo |
Scheme | Entrepreneurs' Programme: Innovation Connections |
Role | Investigator |
Funding Start | 2019 |
Funding Finish | 2019 |
GNo | G1900266 |
Type Of Funding | C2200 - Aust Commonwealth – Other |
Category | 2200 |
UON | Y |
Research Supervision
Number of supervisions
Current Supervision
Commenced | Level of Study | Research Title | Program | Supervisor Type |
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2021 | PhD | Topical, Sustained Release Drug Delivery Platform for the Treatment of Ocular Pain | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
Dr Su Ling Loo
Position
Postdoctoral Research Fellow
Level 2 West
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing