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Home   Researchers   Our researchers
Dr Ran Wang

Dr Ran Wang

Email

ran.wang@mater.uq.edu.au

+61 07 34437659
BioPublications

Dr Ran Wang

Dr Ran Wang was awarded her PhD from The University of Queensland (UQ) in 2015, and after undertaking a postdoc position at Scripps Research in the USA, returned to Australia in 2017 to establish her own research niche. Dr Wang now is a Career Track Fellow at Mater Research, supported by the prestigious Bushell Postdoctoral Research Fellowship from the Gastroenterology Society of Australia.

Ran’s research focuses on diseases that arise as a result of inflammation or infection in the gut and lungs, such as ulcerative colitis and lung fibrosis. She has particular interest on understanding why inflammation happens, and which are the associated consequences to the surrounding tissue (e.g. tissue damage) and other organs (e.g. osteoporosis, muscle wasting). Her longer-term goal is to exploit this knowledge to devise novel therapeutic strategies for treat gut inflammation as well as complications induced by the inflammation.

Inspired by the complex functions of immune cells, Ran aims to engineer decoy “Artificial cells” for understanding the fate of natural immune cells in response to infections and inflammations in human body. Her ultimate goal in this area is to develop a technology combining immunology, material science, with nanotechnology for diagnosis, drug delivery and immune modulation in treating respiratory viral infections, gut inflammations, and autoimmune disorders.

In addition to research, Ran has a passion for communicating her scientific findings to the public and giving back to the community. Ran has been invited to present at 4 international and 6 national conferences. She has been an Associate Editor of Frontiers in Cellular Infection and Molecular Biology since 2018 and contributes to both Australian and New Zealand Society of Immunology, and the Gastroenterology Society of Australia through the organisation of conferences and supporting the administration of the societies. Ran is also passionate about educating the next generation of young scientists via teaching and mentoring. Her has co-supervised two PhD students to completion and had a science student who graduated with Class I Honours as primary supervisor. She is also lecturing at School of Pharmacy, UQ.

“Immunology has always been my interest since I was young. I consider myself lucky to have the opportunity to undertake immunological research as my career. It is where my interest lies, it also excites me when I know that my research findings could potentially benefit patients and the community in the future.”

Research Programs and Groups

  • Chronic Disease Biology and Care - Immunopathology Research

Research Interests

  • Cellular Immunology - Immunology

Publications

The effect of interleukin-22 treatment on autoimmune diabetes in the NOD mouse
2017 - Journal Article - DOI: 10.1007/s00125-017-4392-2
Borg, Danielle J., Wang, Ran, Murray, Lydia, Tong, Hui, Steptoe, Raymond J., McGuckin, Michael A. and Hasnain, Sumaira Z.

Read Abstract

The aim of this study was to determine whether therapy with the cytokine IL-22 could be used to prevent the development of, or treat, autoimmune diabetes in the NOD mouse.


Colonic microbiota can promote rapid local improvement of murine colitis by thioguanine independently of T lymphocytes and host metabolism
2016 - Journal Article - DOI: 10.1136/gutjnl-2015-310874
Oancea, I., Movva, R., Das, I., Aguirre de Carcer, D., Schreiber, V., Yang, Y., Purdon, A., Harrington, B., Proctor, M., Wang, R., Sheng, Y., Lobb, M., Lourie, R., Cuiv, P.O., Duley, J.A., Begun, J. and Florin, T.H.J.

Read Abstract

Objective Mercaptopurine (MP) and pro-drug azathioprine are ‘first-line’ oral therapies for maintaining remission in IBD. It is believed that their pharmacodynamic action is due to a slow cumulative decrease in activated lymphocytes homing to inflamed gut. We examined the role of host metabolism, lymphocytes and microbiome for the amelioration of colitis by the related thioguanine (TG).

Design C57Bl/6 mice with or without specific genes altered to elucidate mechanisms responsible for TG's actions were treated daily with oral or intrarectal TG, MP or water. Disease activity was scored daily. At sacrifice, colonic histology, cytokine message, caecal luminal and mucosal microbiomes were analysed.

Results Oral and intrarectal TG but not MP rapidly ameliorated spontaneous chronic colitis in Winnie mice (point mutation in Muc2 secretory mucin). TG ameliorated dextran sodium sulfate-induced chronic colitis in wild-type (WT) mice and in mice lacking T and B lymphocytes. Remarkably, colitis improved without immunosuppressive effects in the absence of host hypoxanthine (guanine) phosphoribosyltransferase (Hprt)-mediated conversion of TG to active drug, the thioguanine nucleotides (TGN). Colonic bacteria converted TG and less so MP to TGN, consistent with intestinal bacterial conversion of TG to so reduce inflammation in the mice lacking host Hprt. TG rapidly induced autophagic flux in epithelial, macrophage and WT but not Hprt−/− fibroblast cell lines and augmented epithelial intracellular bacterial killing.

Conclusions Treatment by TG is not necessarily dependent on the adaptive immune system. TG is a more efficacious treatment than MP in Winnie spontaneous colitis. Rapid local bacterial conversion of TG correlated with decreased intestinal inflammation and immune activation.


High fat diets induce colonic epithelial cell stress and inflammation that is reversed by IL-22
2016 - Journal Article - DOI: 10.1038/srep28990
Gulhane, Max, Murray, Lydia, Lourie, Rohan, Tong, Hui, Sheng, Yong H., Wang, Ran, Kang, Alicia, Schreiber, Veronika, Wong, Kuan Yau, Magor, Graham, Denman, Stuart, Begun, Jakob, Florin, Timothy H., Perkins, Andrew, Cuiv, Paraic O., McGuckin, Michael A. and Hasnain, Sumaira Z.

Read Abstract

Prolonged high fat diets (HFD) induce low-grade chronic intestinal inflammation in mice, and diets high in saturated fat are a risk factor for the development of human inflammatory bowel diseases. We hypothesized that HFD-induced endoplasmic reticulum (ER)/oxidative stress occur in intestinal secretory goblet cells, triggering inflammatory signaling and reducing synthesis/secretion of proteins that form the protective mucus barrier. In cultured intestinal cells non-esterified long-chain saturated fatty acids directly increased oxidative/ER stress leading to protein misfolding. A prolonged HFD elevated the intestinal inflammatory cytokine signature, alongside compromised mucosal barrier integrity with a decrease in goblet cell differentiation and Muc2, a loss in the tight junction protein, claudin-1 and increased serum endotoxin levels. In Winnie mice, that develop spontaneous colitis, HFD-feeding increased ER stress, further compromised the mucosal barrier and increased the severity of colitis. In obese mice IL-22 reduced ER/oxidative stress and improved the integrity of the mucosal barrier, and reversed microbial changes associated with obesity with an increase in Akkermansia muciniphila. Consistent with epidemiological studies, our experiments suggest that HFDs are likely to impair intestinal barrier function, particularly in early life, which partially involves direct effects of free-fatty acids on intestinal cells, and this can be reversed by IL-22 therapy.


Neutralizing IL-23 is superior to blocking IL-17 in suppressing intestinal inflammation in a spontaneous murine colitis model
2015 - Journal Article - DOI: 10.1097/mib.0000000000000353
Wang, Ran, Hasnain, Sumaira Z., Tong, Hui, Das, Indrajit, Che-Hao Chen, Alice, Oancea, Iulia, Proctor, Martina, Florin, Timothy H., Eri, Rajaraman D. and McGuckin, Michael A.

Read Abstract

Background: IL-23/TH17 inflammatory responses are regarded as central to the pathogenesis of inflammatory bowel disease, but clinically IL-17A antibodies have shown low efficacy and increased infections in Crohn's disease. Hence, we decided to closely examine the role of the IL-23/TH17 axis in 3 models of colitis.

Methods: IL-17A-/- and IL-17Ra-/- T cells were transferred into Rag1-/- and RaW mice to assess the role of IL-17A-IL-17Ra signaling in T cells during colitis. In Winnie mice with spontaneous colitis due to an epithelial defect, we studied the progression of colitis in the absence of IL-17A and the efficacy of neutralizing antibodies against the IL-17A or IL-23p19 cytokines.

Results: In transfer colitis models, IL-17A-deficient T cells failed to ameliorate disease, and IL-17Ra-deficient T cells were more colitogenic than wild-type T cells. In Winnie mice with an epithelial defect and spontaneous TH17-dominated inflammation, genetic deficiency of IL-17A did not suppress initiation of colitis but limited colitis progression. Furthermore, inhibition of IL-17A by monoclonal antibodies did not reduce colitis severity. In contrast, neutralizing IL-23 using an anti-p19 antibody significantly alleviated both emerging and established colitis, downregulating TH17 proinflammatory cytokine expression and diminishing neutrophil infiltration.

Conclusions: Our results support clinical studies showing that IL-17 neutralization is not therapeutic but that targeting IL-23 suppresses intestinal inflammation. Effects of IL-23 distinct from its effects on maturation of IL-17A-producing lymphocytes may underlie the protection from inflammatory bowel disease conveyed by hypomorphic IL-23 receptor polymorphisms and contribute to the efficacy of IL-23 neutralizing antibodies in inflammatory bowel disease.


Targeting IL-23/TH17 axis in suppressing intestinal inflammation
2015 - Thesis - DOI: 10.14264/uql.2015.426
Wang, Ran

no abstract available


Glycemic control in diabetes is restored by therapeutic manipulation of cytokines that regulate beta cell stress
2014 - Journal Article - DOI: 10.1038/nm.3705
Hasnain, Sumaira Z., Borg, Danielle J., Harcourt, Brooke E., Tong, Hui, Sheng, Yonghua H., Ng, Choa Ping, Das, Indrajit, Wang, Ran, Chen, Alice C.-H., Loudovaris, Thomas, Kay, Thomas W., Thomas, Helen E., Whitehead, Jonathan P., Forbes, Josephine M., Prins, Johannes B. and McGuckin, Michael A.

no abstract available


Interleukin-23 mediates the intestinal response to microbial beta-glucan and the development of spondyloarthritis pathology in SKG mice
2014 - Journal Article - DOI: 10.1002/art.38638
Benham, Helen, Rehaume, Linda M., Hasnain, Sumaira Z., Velasco, Jared, Baillet, Athan C., Ruutu, Merja, Kikly, Kristine, Wang, Ran, Tseng, Hsu-Wen, Thomas, Gethin P., Brown, Matthew A., Strutton, Geoffrey, McGuckin, Michael A. and Thomas, Ranjeny

Read Abstract

Objective: Spondyloarthropathies (SpA) occur in 1% of the population, and include ankylosing spondylitis and arthropathy of inflammatory bowel disease (IBD), with characteristic spondylitis, arthritis, enthesitis and IBD. Genetic studies implicate IL-23 receptor signaling in the development of SpA and IBD, and IL-23 over-expression in mice is sufficient for enthesitis, driven by entheseal-resident T cells. However in genetically-prone individuals, it is not clear where IL-23 is produced and how it drives the SpA syndrome, including IBD or sub-clinical gut inflammation of ankylosing spondylitis. Moreover, it is unclear why specific tissue involvement varies between patients with SpA. We determined the location of IL-23 production and its role in SpA pathogenesis in BALB/c ZAP70W163C-mutant (SKG) mice injected i.p. with beta-1,3-glucan (curdlan).

Methods: Eight weeks after curdlan injection of wild type or IL-17-deficient SKG or BALB/c mice, pathology was scored in tissue sections. Mice were treated with anti-IL-23 or anti-IL22. Cytokine production and endoplasmic reticulum stress were determined in affected organs. Results: In curdlan-treated SKG mice arthritis, enthesitis and ileitis were IL-23-dependent. Enthesitis was specifically dependent on IL-17A and IL-22. IL-23 was induced in the ileum, where it amplified endoplasmic reticulum stress, goblet cell dysfunction and pro-inflammatory cytokine production. IL-17A was pathogenic while IL-22 was protective of ileitis. IL-22+CD3- innate-like cells were increased in lamina propria of ileitis-resistant BALB/c mice, which developed ileitis after curdlan and anti-IL-22.

Conclusion: In response to systemic beta-glucan, intestinal IL-23 provokes local mucosal dysregulation and cytokines driving the SpA syndrome, including IL-17/22-dependent enthesitis. Innate IL-22 production promotes ileal tolerance.


MUC1 and MUC13 differentially regulate epithelial inflammation in response to inflammatory and infectious stimuli
2013 - Journal Article - DOI: 10.1038/mi.2012.98
Sheng, Y. H., Triyana, S., Wang, R., Das, I., Gerloff, K., Florin, T. H., Sutton, P. and McGuckin, M. A.

Read Abstract

The MUC1 cell-surface mucin is highly expressed on the gastric mucosal surface, while MUC13 is highly expressed on the intestinal mucosal surface. Polymorphisms in both MUC1 and MUC13 have been linked to inflammatory bowel diseases. MUC1 can act as a decoy molecule on the apical cell surface of epithelial cells and thereby limit bacterial adherence, infection, and inflammation. In this study, we examined whether and how MUC1 and MUC13 modulate infectious and inflammatory signaling. Using gastrointestinal tissue from Muc1- or Muc13-deficient mice in ex vivo culture, MUC1 small interfering RNA (siRNA) silencing in MKN7 gastric epithelial cells, and MUC13 siRNA silencing in LS513 intestinal epithelial cells, we showed that loss of MUC1 increased chemokine secretion, whereas loss of MUC13 decreased chemokine secretion in response to tumor necrosis factor-α. Anti-inflammatory activity of MUC1 and pro-inflammatory activity of MUC13 were also seen after exposure to pathogens, NOD1 (nucleotide-binding oligomerisation domain-containing protein-1), and Toll-like receptor ligands. MUC1 and MUC13 both regulate chemokine secretion in gastrointestinal epithelial cells through a nuclear factor-κB-dependent pathway, although MUC13 modulation could also involve other pathways. Our studies demonstrate that MUC1 and MUC13 are important components of gastrointestinal homeostasis and that disruption or inappropriate expression of these mucins could predispose to infectious and inflammatory disease and inflammation-induced cancer.

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