Dr Ling Chen
School of Biomedical Sciences and Pharmacy
- Phone:(02) 4921 1607
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.
- PhD (Engineering), Chongqing University, China
- Airway remodelling
- Lung development
- Marridan (Maridan) (Mother)
- English (Fluent)
Fields of Research
|060106||Cellular Interactions (incl. Adhesion, Matrix, Cell Wall)||20|
|100404||Regenerative Medicine (incl. Stem Cells and Tissue Engineering)||20|
|Title||Organisation / Department|
|Research Scientist||University of Newcastle
School of Biomedical Sciences and Pharmacy
|Dates||Title||Organisation / Department|
|18/06/2014 - 30/06/2017||
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
For publications that are currently unpublished or in-press, details are shown in italics.
Journal article (16 outputs)
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.
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.
Chen L, Zosky GR, 'Lung development', PHOTOCHEMICAL & PHOTOBIOLOGICAL SCIENCES, 16 339-346 (2017)
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)
Chen L, Wilson R, Bennett E, Zosky GR, 'Identification of vitamin D sensitive pathways during lung development', RESPIRATORY RESEARCH, 17 (2016)
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]
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.
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.
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)
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)
|Show 13 more journal articles|
Conference (14 outputs)
|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)|
|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|
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|