Dr Michaela Finsterbusch, Research Fellow, Centre for Inflammatory Diseases
Platelet accumulation and interactions with neutrophils in acute glomerulonephritis
Glomerulonephritis is a leading cause of end-stage renal failure. In this disease immune cells (e.g. neutrophils in acute glomerulonephritis) are incorrectly activated and start to fight against us by attacking and damaging tissue in the kidney. We believe that cross-talk between different cells (e.g. between platelets and neutrophils) initiate neutrophil-dependent inflammation and the release of harmful factors such as reactive oxygen species. To study the behaviour and distinct role of these cell types in the healthy glomerulus and during acute glomerular inflammation, we use highly advanced microscopy techniques, allowing us to visualise these cells in real-time in the live organ. We hope that data arising from this work will help to better understand the cause of glomerulonephritis and help to develop more effective and saver therapies to block these injurious pathways in patients.
Michaela joined Prof. Michael Hickey's group at the Centre for Inflammatory Diseases, Monash University in 2014 as a research fellow to study immune-modulatory mechanisms of leukocytes in experimental glomerulonephritis. Michaela trained at the University of Applied Sciences in Vienna and graduated with a Master's degree in biomedicine/analytics. During her Master's thesis Michaela studied IL-10 signalling specifically through common IL-10 receptor 1 variants in Prof. Christoph Gasche's lab at the Medical University of Vienna (Department of Gastroenterology). After graduating, Michaela moved to London to do her PhD with Prof. Sussan Nourshargh (William Harvey Research Institute) investigating immune and vascular functions in experimental models of inflammation on a three year British Heart Foundation-funded PhD scholarship. She completed her PhD in 2013 and stayed in London for another year to work in Prof. Amrita Ahluwalia's lab on the transient receptor potential cation channel subfamily V member 1 (TRPV1).
In 2014, Michaela was recruited to Monash University by Prof. Michael Hickey to study the involvement of and communication between different immune cells (e.g. neutrophils, monocytes, platelets) in acute glomerulonephritis. For her work, Michaela primarily uses highly advanced microscopy techniques (i.e. spinning disc and multiphoton confocal microscopy) to visualise different cell types and analyse their behaviour in the live organ.
In 2015, Michaela has been successfully awarded an Erwin Schroedinger fellowship funded by the Austrian Science Fund.
Mr SJ Shen, Postgraduate student, Centre for Inflammatory Diseases – milestone review
Investigating the impact of neutrophil recruitment on colonic inflammation
Inflammatory bowel disease (IBD) is a group of idiopathic, chronic and relapsing inflammatory disease, and includes primarily Crohn’s Disease (CD) and Ulcerative Colitis (UC). There is currently no cure, and disease management strategies only alleviate the symptoms. Patients with IBD have severe complications such as weight loss, fatigue, bloody stools, and diarrhoea. These symptoms arise from activation and potentiation of an abnormal immune response, whereby immune cells are recruited to the gut and damage the gut tissue.
One cell type of interest is neutrophils, where high numbers have been associated with disease. This is also the general consensus in the dextran sodium sulphate (DSS)-induced colitis model, a well-established mouse model of UC, which recapitulates the pathological signs of the human disease.
We now know changes in the gut microbiota affect immune cells such as regulatory T cells and invariant natural killer T (iNKT) cells. Studies have elucidated a clear beneficial role of regulatory T cells in colitis, but the role of iNKT cells is less well-defined. Therefore, the first aim of my project is on exploring the role of iNKT cells on leukocyte recruitment following DSS-induced colitis.
Given the link between the gut microbiota and colitis, modulation of the microbial composition may affect disease progression. In fact, recent research has revealed anti-inflammatory properties of fibre and its fermented products short-chain fatty acids. However, less is known about the impact of a lack of fibre and whether that is a risk factor for the plethora of inflammatory diseases. Thus, the second aim of my project is on examining how a lack of fibre changes the physiology to be more prone to inflammation.
Sj Shen is currently a second year PhD candidate at Monash Medical Centre (Clayton), supervised by Dr. Connie Wong and Prof. Michael Hickey, with a research interest in the effect of dietary fibre in a mouse model of Inflammatory Bowel Disease. He completed Bachelor of Biomedical Sciences at Monash University (Clayton), which included a unit of third year research examining the role of fibre in a mouse model of asthma, taken under the supervision of Dr. Alison Thorburn. Sj then undertook an Honours year with the Department of Immunology (Clayton) at Monash University in the same lab, with research focus on the effect of diet in experimental eosinophilic oesophagitis.
Further information, including the link to add the seminar series to your google calendar, is available from CID Weekly Seminar Series website [http://www.med.monash.edu.au/scs/medicine/cid/seminar-series.html]