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Immune-Vascular Interactions

Blood vessels are the highways that transport our immune cells to sites of inflammation. Our laboratory uses the zebrafish model organism to understand how the behaviour of blood vessels (including growth (angiogenesis) and leakiness (vascular permeability)) affects the function of the immune system. This work will lead to the novel treatments for inflammatory diseases including atherosclerosis, tuberculosis, and meningitis.

The immune-vascular interactions laboratory is currently investigating the following projects:

Imaging atherogenesis
The paradigm of foamy macrophages and lipid accumulation in the walls of blood vessels is well known. However, our understanding of the basic cellular dynamics that take place in atherogenesis has been limited by our inability to image the vessels in which these processes take place with appropriate resolution. We are applying the zebrafish model to characterise immune cell dynamics during atherogenesis, and investigate the importance of vascular remodelling and leakage in fuelling atheroma pathology.

Vascular control of tuberculosis immunity
Angiogenesis, vascular leakiness, and haemostasis are seen around sites of active TB infection called granulomas. We have shown that stopping the growth of blood vessels towards granulomas (anti-angiogenic therapy), inhibition of vascular leakiness, or inhibiting the activation of platelets also reduce mycobacterial growth. Current projects at include determining the mechanism(s) of action of these therapies using a range of experimental models, and validating these therapies into mammalian models of TB infection.

Can the endothelial be a gateway to prevent meningitis?
Cryptococcus neoformans is an opportunistic fungal pathogen responsible for upwards of 600,000 deaths annually and is one of the most deadly infectious afflicting AIDS patients. The related species Cryptococcus gattii is endemic to Australia and capable of causing disease even in immunocompetent people. These fungi home to the central nervous system and are capable of causing severe meningitis even with conventional treatments. Cryptococcal infection of zebrafish can be used to model this process and fungus-immune system interactions can be analysed by live imaging. We want to know if restoring normal vascular function can prevent or reverse the effects of meningitis on the brain.

Dr Stefan Oehlers

Associate Faculty
Phone: +61 2 9565 6192
Email: s.oehlers@centenary.org.au

Stefan trained with the zebrafish as a model of human immunity at the University of Auckland (PhD) and Duke University (postdoc, supported by an NHMRC CJ Martin Fellowship) before moving to Sydney to start an independent lab at the Centenary Institute. His Immune-Vascular Interactions Laboratory primarily seeks to understand how pathology-associated changes to the vasculature affect inflammation. He has an extensive publication record in the fields of mycobacterial infection and inflammatory bowel disease, with additional interests in atherogenesis and diseases with a shared granuloma-like pathotype. Stefan is currently a University of Sydney Fellow with the Marie Bashir Institute and a holder of a NSW Health Early-Mid Career Fellowship.

Dr Elinor Hortle

Research Officer
Email: e.hortle@centenary.org.au

Elinor is a post-doctoral researcher interested in studying the interactions between host and pathogen. She started her research career at the University of Tasmania, before completing her PhD at Macquarie University, studying the effect of genetics on resistance to malaria in mice. She then moved into zebrafish research, and is currently working at the Centenary Institute investigating the ways in which platelets affect tuberculosis infection. Through this research, she hopes to uncover new ways to treat this deadly disease.