12 - 1pm, Tuesday 14 March, Seminar Room 1, TRF Building
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.
AND
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]
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