Identification Of A New Thrombosis Mechanism Triggered By Dying Platelets
Funder
National Health and Medical Research Council
Funding Amount
$608,742.00
Summary
A severe reduction in blood flow (ischemia) to the intestines can trigger blood clot formation (thrombosis) in multiple organs, including the lungs. We have identified a new thrombosis mechanism that is triggered by the clumping of white blood cells in the intestines, leading to widespread thrombosis in the lung. Here we will investigate the mechanisms triggering this thrombosis mechanism with the ultimate aim of identifying more effective antithrombotic approaches.
Modulation Of Endothelial Junctions As Selective Immunotherapy
Funder
National Health and Medical Research Council
Funding Amount
$911,387.00
Summary
We have developed a new drug (CD5-2) that targets the junctions of endothelial cells, the cell that lines all vessels. CD5-2 reduces oedema in diseases such as diabetic retinopathy and tumours. Thus it has potential as a new therapeutic in chronic inflammatory diseases where leaky blood vessels are central to the pathology. This grant will provide fundamental understanding of how CD5-2 induces such profound effects to alter the levels of oedema and alter inflammatory cell infiltrates in tissues.
First-in-Field Study Of Mechanisms Operating In Post-Ebola Eye Disease
Funder
National Health and Medical Research Council
Funding Amount
$748,985.00
Summary
Ebola virus disease is a life-threatening illness with no treatment. Survivors of the disease are at risk of uveitis - inflammation inside the eye - related to the ability of Ebola virus to persist in the eye. Our research will examine the cellular and molecular events that occur in an eye that harbours Ebola virus. This work will be an important step towards the development of treatments for uveitis caused by Ebola virus.
Mast cells (MC) are key regulators of chronic skin inflammation, such as atopic eczema, and can also give rise to a group of diseases called mastocytosis. How MC numbers are regulated in these conditions is poorly understood. We have identified a novel circulating precursor cell that gives rise to MC. We will determine the function of these precursors in skin diseases, including eczema and mastocytosis, with the aim to curtail the course of of these difficult-to-treat conditions.
Cellular And Molecular Mechanisms Of Fungal Infection Pathogenesis And Therapy
Funder
National Health and Medical Research Council
Funding Amount
$561,028.00
Summary
Fungal infections are serious problems for patients with depressed immunity such as chemotherapy or transplant patients. More effective antifungal treatments are needed. We will study a model of fungal infection in zebrafish embryos that recapitulates human penicilliosis. The research will study how the infection establishes and how different types of white blood cells either help or hinder infection establishment. The results will point to new approaches for treating serious fungal infections.
Inflammatory Pathways For Novel Therapeutic Interventions In Preterm Delivery
Funder
National Health and Medical Research Council
Funding Amount
$568,006.00
Summary
Preterm birth is common and carries severe risks for the child. Existing therapies are not very successful in arresting preterm labour or improving outcomes for the fetus. We have discovered that blocking inflammatory ‘sensor’ molecules can slow labour progression. This project will (1) increase our knowledge of the inflammatory pathways that initiate early labour, and (2) define the mechanism of action and safety of a new drug that has potential for delaying preterm birth in women.
Activating T Cell Tolerance To Prevent Preeclampsia
Funder
National Health and Medical Research Council
Funding Amount
$632,000.00
Summary
Preeclampsia is a leading cause of prematurity and low birth weight in babies. There is evidence that preeclampsia originates with inadequate adaptation in the mother’s immune system to protect the placenta from immune attack. In mice we will investigate how events at conception activate immune tolerance, and define how the male partner contributes. In women, we will determine whether similar processes control the immune response in pregnancy, and whether this is faulty in preeclampsia.