Dr Ling Chen

Dr Ling Chen

Research Scientist

School of Biomedical Sciences and Pharmacy

Career Summary

Biography

Dr Chen has a PhD in Biomedical Engineering from Chongqing University, China (2014) and a master in Sport Physiology from Chengdu Sports University, China (2010). While Dr Chen was working on her PhD degree, she had two years years PhD research training at Woolcock Institute of Medical Research, Sydney (2011-2013). During the two years training in Sydney, Dr Chen has gained her skills on primary lung cell culture and studied the mechanism of airway tissue remodelling in Chronic Obstructive Pulmonary Disease (COPD). Dr Chen started her professional career at the University of Tasmania as a Postdoctoral Research Fellow (2014-2017), where she has established her expertise in paediatric lung development and environmental effects on lung health. In July 2017, Dr Chen joined Hunter Medical Research Institute at the University of Newcastle, Australia and work with Laureate Professor Paul Foster and Dr Gerard Kaiko. Dr Chen’s research interests include investigating the pathophysiology of severe asthma, COPD and pulmonary fibrosis, and developing therapeutical approaches.


Qualifications

  • PhD (Engineering), Chongqing University, China

Keywords

  • Airway remodelling
  • Asthma
  • COPD
  • Immunology
  • Lung development

Languages

  • Marridan (Maridan) (Mother)
  • English (Fluent)

Fields of Research

Code Description Percentage
110203 Respiratory Diseases 60
060106 Cellular Interactions (incl. Adhesion, Matrix, Cell Wall) 20
100404 Regenerative Medicine (incl. Stem Cells and Tissue Engineering) 20

Professional Experience

UON Appointment

Title Organisation / Department
Research Scientist University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Professional appointment

Dates Title Organisation / Department
18/06/2014 - 30/06/2017 Research fellow

Dr Ling Chen was a Postdoctoral Research Fellow at the School of Medicine in the faculty of healthy. Her reserach interests are focus on respiratory health and lung diseases.

University of Tasmania
School of Medicine
Australia
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Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Journal article (16 outputs)

Year Citation Altmetrics Link
2018 Chen L, Bennett E, Wheeler AJ, Lyons AB, Woods GM, Johnston F, Zosky GR, 'Maternal exposure to particulate matter alters early post-natal lung function and immune cell development', Environmental Research, 164 625-635 (2018) [C1]

© 2018 Elsevier Inc. Background: In utero exposure to particulate matter (PM) from a range of sources is associated with adverse post-natal health; however, the effect of maternal... [more]

© 2018 Elsevier Inc. Background: In utero exposure to particulate matter (PM) from a range of sources is associated with adverse post-natal health; however, the effect of maternal exposure to community-sampled PM on early post-natal lung and immune development is poorly understood. Objectives: Using a mouse model, we aimed to determine whether in utero exposure to PM alters early post-natal lung function and immune cell populations. We used PM collected from ceiling voids in suburban houses as a proxy for community PM exposure. Methods: Pregnant C57BL/6 mice were intranasally exposed to ceiling derived PM, or saline alone, at gestational day (E) 13.5, 15.5, and 17.5. When mice were two weeks old, we assessed lung function by the forced oscillation technique, and enumerated T and B cell populations in the spleen and thymus by flow cytometry. Results: Maternal exposure to PM impaired somatic growth of male offspring resulting in reduced lung volume and deficits in lung function. There was no effect on thymic T cell populations in dams and their male offspring but PM decreased the CD4 +CD25 + T cell population in the female offspring. In contrast, maternal exposure to PM increased splenic CD3 +CD4 + and CD3 +CD8 + T cells in dams, and there was some evidence to suggest inhibition of splenic T cell maturation in male but not female offspring. Conclusions: Our findings suggested that maternal exposure to ceiling void PM has the capacity to impair early somatic growth and alter early life immune development in a sex specific manner.

DOI 10.1016/j.envres.2018.03.029
2018 Shao J, Wheeler AJ, Chen L, Strandberg B, Hinwood A, Johnston FH, Zosky GR, 'The pro-inflammatory effects of particulate matter on epithelial cells are associated with elemental composition', Chemosphere, 202 530-537 (2018)

© 2018 Elsevier Ltd Background: Adverse health effects of particulate matter (PM) vary with chemical composition; however, evidence regarding which elements are the most detriment... [more]

© 2018 Elsevier Ltd Background: Adverse health effects of particulate matter (PM) vary with chemical composition; however, evidence regarding which elements are the most detrimental is limited. The roof space area provides an open and stable environment for outdoor PM to settle and deposit. Therefore, this study used roof space PM samples as a proxy of residential cumulative exposure to outdoor air pollution to investigate their pro-inflammatory effects on human lung cells and the contribution of the endotoxin and chemical content. Methods: Roof space PM samples of 36 different homes were collected and analysed using standardised techniques. We evaluated cytotoxicity and cytokine production of BEAS-2B cells after PM exposure using MTS and ELISA, respectively. Principle component analysis (PCA) and linear regression analyses were employed to assess the associations between cytokine production and the PM components. Results: PM caused significant time- and dose-dependent increases in cellular cytokine production (p < 0.05). PCA identified four factors that explained 68.33% of the variance in the chemical composition. An increase in Factor 1 (+Fe, +Al, +Mn) score and a decrease in Factor 2 (-Ca, +Pb, +PAH) score were associated with increased interleukin (IL)-6 (Factor 1; p = 0.010; Factor 2; p = 0.006) and IL-8 (Factor 1; p = 0.003; Factor 2; p = 0.020) production, however, only the association with Factor 1 was evident after correcting for endotoxin and particle size. Conclusions: Our study provides novel insight into the positive associations between pro-inflammatory effects of roof space PM samples with Fe, Al and Mn levels.

DOI 10.1016/j.chemosphere.2018.03.052
2017 Chen L, Zosky GR, 'Lung development', PHOTOCHEMICAL & PHOTOBIOLOGICAL SCIENCES, 16 339-346 (2017)
DOI 10.1039/c6pp00278a
Citations Scopus - 1Web of Science - 1
2017 Chen L, Eapen M, Zosky G, 'Vitamin D both facilitates and attenuates the cellular response to lipopolysaccharide', Scientific Reports, 7 45172-45172 (2017)
DOI 10.1038/srep45172
2017 Nuñez NK, Bennett E, Chen L, Pitrez PM, Zosky GR, 'The independent effects of Vitamin D deficiency and house dust mite exposure on lung function are sex-specific', Scientific Reports, 7 (2017)

© 2017 The Author(s). Vitamin D deficiency is increasing around the world and has been associated with the development of asthma. This study aims to evaluate the effect of dietary... [more]

© 2017 The Author(s). Vitamin D deficiency is increasing around the world and has been associated with the development of asthma. This study aims to evaluate the effect of dietary vitamin D deficiency at different life stages on lung function using a murine model of allergic airways disease. BALB/c mice were challenged intranasally with HDM or saline alone for 10 days. Twenty four hours after the last challenge, mice were anesthetized and lung function was measured using the forced oscillation technique (FOT). Mice were euthanized for assessment of inflammation in the bronchoalveolar lavage (BAL) and total collagen content in lung homogenates by ELISA. Vitamin D deficiency impaired lung function in both male and female mice, increasing tissue damping and elastance, however had no effect on HDM induced inflammation. The impact of vitamin D deficiency was more evident in females. HDM also decreased airway distensibility, but only in females and this response was not altered by vitamin D deficiency. Our data suggest that vitamin D deficiency and HDM exposure have independent effects on lung mechanics and that females are more susceptible to these effects. Vitamin D deficiency may exacerbate lung function deficits by having a direct, but independent, effect on parenchymal mechanics.

DOI 10.1038/s41598-017-15517-z
2017 Williams LJ, Chen L, Zosky GR, 'The respiratory health effects of geogenic (earth derived) PM

© 2017 Informa UK Limited, trading as Taylor &amp; Francis Group. Inhalation of particulate matter less than 10¿µm in diameter (PM10) has a range of implications for respiratory... [more]

© 2017 Informa UK Limited, trading as Taylor & Francis Group. Inhalation of particulate matter less than 10¿µm in diameter (PM10) has a range of implications for respiratory health. In order to mitigate these effects regulatory bodies have set ambient air quality guidelines based on the known dose¿response relationships between PM10exposure and health outcomes. However, these data are based almost entirely on PM10from urban regions, which are typically dominated by particulates from combustion sources. In contrast, there are limited data on the respiratory health effects of particles from nonurban regions that often contain a high geogenic (earth derived) component. In this narrative review, we summarize the existing evidence for the respiratory health effects of inhalation of geogenic PM10.We outline the impact of physicochemical properties on the lung response, with a view to identifying gaps in the field.

DOI 10.1080/08958378.2017.1367054
2016 Chen L, Wilson R, Bennett E, Zosky G, 'Identification Of Vitamin D Sensitive Pathways During Lung Development', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 193 (2016)
Citations Scopus - 9
2016 Chen L, Wilson R, Bennett E, Zosky GR, 'Identification of vitamin D sensitive pathways during lung development', RESPIRATORY RESEARCH, 17 (2016)
DOI 10.1186/s12931-016-0362-3
Citations Web of Science - 11
2015 Chen L, Jiang X, Deng L, 'effects of cigarette smoke in primary human lung cells influencing airway remodeling of chronic obstructive pulmonary disease', Chinese Journal of Gerontology, 12 289-292 (2015)
2015 Ge Q, Chen L, Jaffar J, Argraves WS, Twal WO, Hansbro P, et al., 'Fibulin1C peptide induces cell attachment and extracellular matrix deposition in lung fibroblasts', SCIENTIFIC REPORTS, 5 (2015) [C1]
DOI 10.1038/srep09496
Citations Scopus - 12Web of Science - 12
Co-authors Philip Hansbro
2014 Chen L, Ge Q, Tjin G, Alkhouri H, Deng L, Brandsma CA, et al., 'Effects of cigarette smoke extract on human airway smooth muscle cells in COPD', European Respiratory Journal, 44 634-646 (2014)

We hypothesised that the response to cigarette smoke in airway smooth muscle (ASM) cells from smokers with chronic obstructive pulmonary disease (COPD) would be intrinsically diff... [more]

We hypothesised that the response to cigarette smoke in airway smooth muscle (ASM) cells from smokers with chronic obstructive pulmonary disease (COPD) would be intrinsically different from smokers without COPD, producing greater pro-inflammatory mediators and factors relating to airway remodelling. ASM cells were obtained from smokers with or without COPD, and then stimulated with cigarette smoke extract (CSE) or transforming growth factor-ß1. The production of chemokines and matrix metalloproteinases (MMPs) were measured by ELISA, and the deposition of collagens by extracellular matrix ELISA. The effects of CSE on cell attachment and wound healing were measured by toluidine blue attachment and cell tracker green wound healing assays. CSE increased the release of CXCL8 and CXCL1 from human ASM cells, and cells from smokers with COPD produced more CSE-induced CXCL1. The production of MMP-1, -3 and -10, and the deposition of collagen VIII alpha 1 (COL8A1) were increased by CSE, especially in the COPD group which had higher production of MMP-1 and deposition of COL8A1. CSE decreased ASM cell attachment and wound healing in the COPD group only. ASM cells from smokers with COPD were more sensitive to CSE stimulation, which may explain, in part, why some smokers develop COPD. Copyright ©ERS 2014.

DOI 10.1183/09031936.00171313
Citations Scopus - 11Web of Science - 9
2014 Ojo O, Lagan AL, Rajendran V, Spanjer A, Chen L, Sohal SS, et al., 'Pathological changes in the COPD lung mesenchyme - Novel lessons learned from invitro and invivo studies', Pulmonary Pharmacology and Therapeutics, 29 121-128 (2014)

© 2014 Elsevier Ltd. Chronic obstructive pulmonary disease (COPD) is currently the fourth leading cause of death worldwide and, in contrast to the trend for cardiovascular disease... [more]

© 2014 Elsevier Ltd. Chronic obstructive pulmonary disease (COPD) is currently the fourth leading cause of death worldwide and, in contrast to the trend for cardiovascular diseases, mortality rates still continue to climb. This increase is in part due to an aging population, being expanded by the "Baby boomer" generation who grew up when smoking rates were at their peak and by people in developing countries living longer. Sadly, there has been a disheartening lack of new therapeutic approaches to counteract the progressive decline in lung function associated with the disease that leads to disability and death. COPD is characterized by irreversible chronic airflow limitation that is caused by emphysematous destruction of lung elastic tissue and/or obstruction in the small airways due to occlusion of their lumen by inflammatory mucus exudates, narrowing and obliteration. These lesions are mainly produced by the response of the tissue to the repetitive inhalational injury inflicted by noxious gases, including cigarette smoke, which involves interaction between infiltrating inflammatory immune cells, resident cells (e.g. epithelial cells and fibroblasts) and the extra cellular matrix. This interaction leads to tissue destruction and airway remodeling with changes in elastin and collagen, such that the epithelial-mesenchymal trophic unit is dysregulated in both the disease pathologies. This review focuses on: 1 - novel inflammatory and remodeling factors that are altered in COPD; 2 - invitro and invivo models to understand the mechanism whereby the extra cellular matrix environment in altered in COPD; and 3 - COPD in the context of wound-repair tissue responses, with a focus on the regulation of mesenchymal cell fate and phenotype.

DOI 10.1016/j.pupt.2014.04.004
Citations Scopus - 19Web of Science - 17
2014 Chen L, Perks KL, Stick SM, Kicic A, Larcombe AN, Zosky G, 'House Dust Mite Induced Lung Inflammation Does Not Alter Circulating Vitamin D Levels', PLOS ONE, 9 (2014)
DOI 10.1371/journal.pone.0112589
Citations Scopus - 4Web of Science - 3
2013 Chen L, Ge Q, Black JL, Deng L, Burgess JK, Oliver BGG, 'Differential Regulation of Extracellular Matrix and Soluble Fibulin-1 Levels by TGF-beta(1) in Airway Smooth Muscle Cells', PLOS ONE, 8 (2013)
DOI 10.1371/journal.pone.0065544
Citations Scopus - 13Web of Science - 4
2012 Chen L, Sun C, Deng L, 'The study of ß2-adrenergic receptor gene polymorphism in Sanda athletes', Sheng Wu Yi Xue Gong Cheng Xue Za Zhi, 29 129-133 (2012)
2011 Chen L, 'ß2-adrenergic receptor gene polymorphism and asthma', Modern Preventive Medicine, 38 1591-1593 (2011)
Show 13 more journal articles

Conference (14 outputs)

Year Citation Altmetrics Link
2017 Chen L, Bennett E, Wheeler A, Johnston F, Zosky G, 'Effect Of In Utero Exposure To Ceiling Particles On Post-Natal Lung Function And Immune Cell Populations', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Washington, DC (2017)
2017 Chen L, Bennett E, Wheeler A, Johnston F, Zosky G, 'EFFECT OF IN UTERO EXPOSURE TO CEILING PARTICLES ON POST-NATAL LUNG FUNCTION', RESPIROLOGY (2017)
2017 Chen L, Bennett E, Wheeler A, Johnston F, Zosky G, 'EFFECT OF IN UTERO EXPOSURE TO CEILING PARTICLES ON THE EARLY POST-NATAL IMMUNE CELL POPULATIONS', RESPIROLOGY (2017)
2017 Williams L, Chen L, Zosky G, 'THE IMPACT OF IRON OXIDE AND SILICA ON INFLAMMATORY RESPONSES IN BEAS-2B CELLS', RESPIROLOGY (2017)
2016 Chen L, Wilson R, Bennett E, Zosky G, 'IMPACTS OF MATERNAL VITAMIN D DEFICIENCY ON LUNG DEVELOPMENT', RESPIROLOGY (2016)
2015 Chen L, Foong R, Bennett E, Zosky G, 'IN UTERO VITAMIN D DEFICIENCY ALTERS THE EXPRESSION OF MMP8 IN FOETAL LUNG', RESPIROLOGY, Queensland, AUSTRALIA (2015)
2014 Ge Q, Chen L, Jaffar J, Black JL, Burgess JK, Oliver BG, 'The Role Of Fibulin-1c Peptides In Attachment, Proliferation And Ecm Deposition In Lung Fibroblasts From Chronic Lung Diseases', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2014)
2014 Ge Q, Chen L, Jaffar J, Black J, Burgess J, Oliver B, 'FIBULIN-1C PEPTIDE INDUCES CELL ATTACHMENT, PROLIFERATION AND ECM DEPOSITION IN LUNG FIBROBLAST', RESPIROLOGY (2014)
2013 Chen L, Ge Q, Black J, Burgess J, Oliver B, 'Cigarette smoke extract and TGF-beta(1) induce distinctive expression of extracellular matrix protein genes in human airway smooth muscle cells', EUROPEAN RESPIRATORY JOURNAL (2013)
2013 Chen L, Ge Q, Black JL, Burgess JK, Oliver BG, 'Difference Between Matrix And Soluble Fibulin-1 In Airway Smooth Muscle Cells', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2013)
2013 Ge Q, Jaffar J, Chen L, Black JL, Burgess JK, Oliver BG, 'Identification Of The Active Region Of Fibulin1 In Remodelling And Inflammation In Lung Fibroblasts', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2013)
2013 Chen L, Ge Q, Faiz A, Black JL, Burgess JK, Oliver BG, 'Cigarette Smoke Extract And Tgf-beta 1 Induce Distinctive Expression Of Extracellular Matrix And Adhesion Molecule Genes In COPD And Non-COPD Airway Smooth Muscle Cells', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2013)
2013 Chen L, Ge Q, Black JL, Burgess JK, Oliver BGG, 'DIFFERENCES BETWEEN DEPOSITED AND SOLUBLE FIBULIN-1 IN AIRWAY SMOOTH MUSCLE CELLS', RESPIROLOGY (2013)
2013 Ge Q, Jaffar J, Chen L, Black JL, Burgess JK, Oliver B, 'THE ROLE OF FIBULIN-1 PEPTIDES IN LUNG FIBROBLAST ASSOCIATED REMODELLING AND INFLAMMATION', RESPIROLOGY (2013)
Show 11 more conferences
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Grants and Funding

Summary

Number of grants 1
Total funding $25,000

Click on a grant title below to expand the full details for that specific grant.


20181 grants / $25,000

Mini-organs in a dish: a personalised test for cystic fibrosis treatment to reduce the need for lung transplantation$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Gerard Kaiko, Doctor Ling Chen, Conjoint Professor Peter Wark
Scheme Project Grant
Role Investigator
Funding Start 2018
Funding Finish 2018
GNo G1801337
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y
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Research Collaborations

The map is a representation of a researchers co-authorship with collaborators across the globe. The map displays the number of publications against a country, where there is at least one co-author based in that country. Data is sourced from the University of Newcastle research publication management system (NURO) and may not fully represent the authors complete body of work.

Country Count of Publications
Australia 26
China 5
United Kingdom 2
Netherlands 2
United States 2
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Dr Ling Chen

Position

Research Scientist
Paul Foster's group
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Contact Details

Email ling.chen@newcastle.edu.au
Phone (02) 4921 1607

Office

Room HMRI L2E 2403
Building HMRI
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