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Pulmonary Artery Pulsatility As A Predictor Of Survival Following Hospitalized Exacerbation Of Chronic Obstructive Pulmonary Disease
Funder
National Health and Medical Research Council
Funding Amount
$128,224.00
Summary
Many patients with Chronic Obstructive Pulmonary Disease (COPD) also have elevated lung blood pressures, or pulmonary hypertension (PH). Having both conditions increases the risk of death. It is difficult to diagnose PH in COPD. We will be using a new Computed Tomography (X-ray imaging) technique to investigate a marker of PH called ‘pulmonary artery pulsatility’. If PH can be diagnosed easily and accurately new treatments can be devised and researched potentially improving outcomes in COPD.
Preventing Complications Of Chronic Obstructive Pulmonary Disease
Funder
National Health and Medical Research Council
Funding Amount
$310,914.00
Summary
Chronic obstructive pulmonary disease (COPD) is a devastating lung disease that affects smokers. Lung complications and complications in other organs occur commonly. This study will examine factors that lead to exacerbations of COPD, and test the effectiveness of early diagnosis of coronary artery disease using CT scans.
Targeting IL-33 In Chronic Obstructive Pulmonary Disease (COPD), Chronic Asthma And Idiopathic Pulmonary Fibrosis (IPF)
Funder
National Health and Medical Research Council
Funding Amount
$318,768.00
Summary
Lung diseases (emphysema, severe asthma & pulmonary fibrosis) are major burdens on Australian community and economy. Airway wounding is a key feature of all these diseases. Patients experience severe breathlessness seriously impacting quality of life and frequently leading to death. We will assess the potential of a new target (IL-33), & therapy (anti-IL-33) in suppressing wounding in experimental models and human tissues. This may lead to a new treatment to reverse and/or prevent lung diseases.
This program of work focuses on smoking related lung diseases including chronic bronchitis and emphysema, and lung cancer, as well as diseases affecting the blood vessels in the lungs. The work includes basic cell biology and human clinical trials.There is a high likelihood that new approaches to treating lung disease will emerge.
Elucidating The Role And Potential For Therapeutic Targeting Of TLR7 In Emphysema And COPD
Funder
National Health and Medical Research Council
Funding Amount
$925,780.00
Summary
Emphysema is a major cause of illness and death and there are no effective treatments. It is caused by smoking that damages the airways and air sacs but how this occurs is not well understood. We have found that a new factor, called Toll-like receptor 7, is involved in emphysema. In this study we will now characterise its roles in this disease, work out how it induces emphysema and test new inhibitors (antibodies) that we have developed as treatments.
Modulation Of Macrophage Function As A Therapy For Chronic Obstructive Pulmonary Disease (COPD)
Funder
National Health and Medical Research Council
Funding Amount
$435,589.00
Summary
We have established that defective clearance of dying cells by phagocytes in the airway can a) perpetuate inflammation in smokers with-without COPD and b) be improved by administration of therapies (Mannose binding lectin and Procysteine) in a mouse model. The current proposal specifically addresses the role of phagocytes in the ongoing airway damage in our COPD patients, and more thoroughly investigates the mechanisms and effects of administration of relevant new therapies (in a mouse model).
Enhancing Innate Immune Responses To Influenza In Chronic Obstructive Pulmonary Disease
Funder
National Health and Medical Research Council
Funding Amount
$522,323.00
Summary
Infection with influenza is a serious health problem for all, but particularly those with chronic lung diseases such as chronic obstructive pulmonary disease (COPD). Current treatments are limited. We have previously shown that human COPD airway cells are more susceptible to infection with influenza and the virus is able to effectively block the early immune response. We propose to define the mechanism that underlie this and design novel inhibitors to enhance the early immune response of these c ....Infection with influenza is a serious health problem for all, but particularly those with chronic lung diseases such as chronic obstructive pulmonary disease (COPD). Current treatments are limited. We have previously shown that human COPD airway cells are more susceptible to infection with influenza and the virus is able to effectively block the early immune response. We propose to define the mechanism that underlie this and design novel inhibitors to enhance the early immune response of these cells and reduce the effects of infection.Read moreRead less
Understanding The Role Of Th22 Cells In Regulating Respiratory Immune Responses In Health And Disease.
Funder
National Health and Medical Research Council
Funding Amount
$870,476.00
Summary
T cells that produce the cytokine IL-22 (Th22 cells) are found in infectious and inflammatory lung disease. However, the role of Th22 cells in promoting or preventing disease remains largely unknown. We have discovered how to grow Th22 cells and have generated a unique strain of IL-22 reporter mice, which will allow us to identify their role in infectious and inflammatory diseases. Our investigations will provide new insights into therapeutic approaches for these diseases of the lung.
Defining The Roles And Targeting Interferon-epsilon As A New Therapy For Influenza In Asthma And COPD
Funder
National Health and Medical Research Council
Funding Amount
$905,904.00
Summary
Influenza is a major cause of illness and death, especially in people with asthma and emphysema. There are issues with vaccines and current treatments are poorly effective. Effective treatments are urgently required. We have found a new immune factor, interferon-epsilon that is induced and used by influenza viruses to cause infection. We aim to understand how this occurs and to test new treatments for influenza that suppress interferon-epsilon, in healthy and susceptible individuals.