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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).
Identifying New Therapeutic Targets For Preventing The Induction And Progression Of COPD
Funder
National Health and Medical Research Council
Funding Amount
$649,314.00
Summary
Smoking leads to lung inflammation that causes emphysema, which is a major health problem in Australia. Once induced there is a progressive decline in health, which continues even after stopping smoking. There are no treatments that halt this decline. Recently small genes have been discovered that control inflammation. We may be able to control these small genes and stop the induction and progression of emphysema. This project may lead to a completely new way of preventing and treating emphysema ....Smoking leads to lung inflammation that causes emphysema, which is a major health problem in Australia. Once induced there is a progressive decline in health, which continues even after stopping smoking. There are no treatments that halt this decline. Recently small genes have been discovered that control inflammation. We may be able to control these small genes and stop the induction and progression of emphysema. This project may lead to a completely new way of preventing and treating emphysema.Read moreRead less
Chronic obstructive pulmonary disease (COPD) is a major global health problem and has been predicted to become the third largest cause of death in the world by 2020. Cigarette smoking is the major cause of COPD and accounts for more than 95% of cases in industrialized countries. Cigarette smoke triggers cells in the lung to release substances which cause inflammation and eat away lung tissue. In addition, these substances enter the blood and muscle where they eat away muscle resulting in signifi ....Chronic obstructive pulmonary disease (COPD) is a major global health problem and has been predicted to become the third largest cause of death in the world by 2020. Cigarette smoking is the major cause of COPD and accounts for more than 95% of cases in industrialized countries. Cigarette smoke triggers cells in the lung to release substances which cause inflammation and eat away lung tissue. In addition, these substances enter the blood and muscle where they eat away muscle resulting in significant weight loss. Patients with COPD have severe difficulty in breathing because the lungs are damaged and do not function properly. This process, once started, cannot be reversed and there is currently no satisfactory therapy to help treat individuals with this terrible disease. People with COPD are prone to viral and bacterial infections of the lungs. These infections cause further inflammation, lung damage and difficulty in breathing. These infections place a tremendous burden on health care resources, have a huge effect on the quality of life and are a common cause of death. The reason why respiratory infections are so serious for people with COPD is unclear. Preliminary results from our laboratory show that a substance called GM-CSF, released from cells in the lung, may be involved in the development of COPD. Thus, the aim of this project is to use our mouse models of COPD to determine whether GM-CSF is involved in the development of COPD. The insights gained may lead to the identification of potentially novel ways to prevent and treat COPD.Read moreRead less
Surfactant Protein D As A Candidate Therapy In COPD
Funder
National Health and Medical Research Council
Funding Amount
$405,749.00
Summary
Smoking -related chronic bronchitis and emphysema, otherwise known COPD, costs the healthcare system over $800 million per year. People continue to suffer even after they have given up smoking, and the treatments available result in only modest improvements. COPD is associated with a a defect of the scavenging cells in the lung, which normally clear away dying cells, and some of the proteins ivolved in this process. We will investigate whether supplementing these proteins will help.
The Role Of Apoptosis And Macrophage Function In Chronic Obstructive Pulmonary Disease
Funder
National Health and Medical Research Council
Funding Amount
$463,400.00
Summary
Chronic obstructive pulmonary disease (COPD) is a complex, chronic disease of the lungs principally caused by cigarette smoking. COPD is very common and causes a great deal of debility and mortality in our community. COPD is also linked to an increased risk of lung cancer and carviovascular disease. It is estimated to cost Australians at least $800 million dollars per year in health related costs. Despite its importance, there is a limited understanding of how COPD develops and treatment options ....Chronic obstructive pulmonary disease (COPD) is a complex, chronic disease of the lungs principally caused by cigarette smoking. COPD is very common and causes a great deal of debility and mortality in our community. COPD is also linked to an increased risk of lung cancer and carviovascular disease. It is estimated to cost Australians at least $800 million dollars per year in health related costs. Despite its importance, there is a limited understanding of how COPD develops and treatment options are limited. We have identified large numbers of dying cells in the airways of people with COPD and we believe that these play a critical part in the cause and-or progression of the illness. This project will determine whether the increased rates of cell death are the result of the COPD process or part of the actual cause of the disease. This knowledge will enable us to address the urgent need to predict the risk of developing COPD in current and ex- smokers. Cells obtained from the lungs of healthy controls, current- ex smokers without COPD and current- ex smokers with COPD will be studied. The effects of current treatments for COPD on these cells as well as testing novel treatments will also be studied, paying particular attention to the effects on cell death. In this way we hope that new therapies will be identified to improve the health and well-being of those with COPD.Read moreRead less
Molecular Mechanisms Of Wasting In Experimental COPD
Funder
National Health and Medical Research Council
Funding Amount
$389,521.00
Summary
Chronic obstructive pulmonary disease (COPD) is a major global health problem and has been predicted to become the third largest cause of death in the world by 2020. Cigarette smoking is the major cause of COPD and accounts for more than 95% of cases in industrialized countries. Currently no therapies exist to halt the inevitable progression of the disease. To date most of the research has focused on the aspects of this disease which result in destruction of the lung however it is becoming incre ....Chronic obstructive pulmonary disease (COPD) is a major global health problem and has been predicted to become the third largest cause of death in the world by 2020. Cigarette smoking is the major cause of COPD and accounts for more than 95% of cases in industrialized countries. Currently no therapies exist to halt the inevitable progression of the disease. To date most of the research has focused on the aspects of this disease which result in destruction of the lung however it is becoming increasingly evident that COPD is a disease of multiple organs. Until recently it had been widely believed that the profound loss of exercise tolerance observed in COPD patients was due to impaired gas exchange secondary to lung structural damage. Loss of lean body mass (muscle) is now recognised as a major co-morbidity of COPD and a direct cause of functional impairment with patients suffering marked deteriorations in quality of life, increased mortality, breathlessness and decreased exercise tolerance. Skeletal muscle wasting is a powerful predictor of mortality in COPD, independent of the lung function impairment. Despite the clinical seriousness of muscle wasting and suggestive evidence that it may be reversible, little is known about the pathogenic mechanisms. Therefore the goal of this project is to use experimental models of COPD to identify the molecular basis of wasting, in order to restore skeletal muscle homeostasis. The insights gained from this research proposal may lead to the identification of potentially novel targets for the prevention and reversal of the debilitating and life threatening effects of skeletal muscle wasting in COPD. For the COPD patient this has the potential to increase quality of life, functional ability and life expectancy.Read moreRead less
Scarring And Angiogenesis In The Airway Wall In Smoking And COPD: Links Between Inflammation And Remodelling
Funder
National Health and Medical Research Council
Funding Amount
$361,614.00
Summary
Smoking damages airways to produce scarring and new blood vessel growth resulting in airway narrowing, so-called COPD. Details of these processes are poorly understood. We will analyse airway biopsies taken from smokers, to dissect out the linkages between airway damage, airway inflammation, structural remodelling, and clinical changes. We will investigate the effects on these processes of: 1) inhaled corticosteroid; and 2) smoking cessation over 3 and 12 months.
Optimising Outcomes For Chronic Obstructive Pulmonary Disease (COPD): Evaluation Of Walking Training.
Funder
National Health and Medical Research Council
Funding Amount
$440,161.00
Summary
This will be the first study to examine whether a short-term and long-term program of ground walking training is sufficient to improve and maintain exercise capacity and quality of life in people with COPD. If ground walking training is shown to be an effective intervention, this will translate into more widespread provision of exercise training to people with COPD, particularly those living in rural or remote communities.
Restoring Skeletal Muscle In An Experimental Model Of COPD By Targeting The IGF-1-myostatin-macrophage Axis
Funder
National Health and Medical Research Council
Funding Amount
$508,183.00
Summary
Most people think that the serious disabilities of COPD (emphysema) patients follows damage to their lungs but wasted muscles may be even more important. We can not regrow lung but we have found a way that might help regrow muscle. We plan to use stem cells to make one of the body's own cells called 'macrophages' and genetically engineer these cells to help deliver healing proteins directly into the muscle. Making muscle stronger will help COPD patients live longer and improve quality of life.
Genetic Dissection Of The Function Of The Src Family Tyrosine Kinase Hck In Inflammatory Lung Disease
Funder
National Health and Medical Research Council
Funding Amount
$323,750.00
Summary
This project aims to identify better and safer treatments for serious, life-threatening inflammatory lung diseases, such as Chronic Obstructive Lung Disease (COPD), which affect over 600 million people worldwide and are a major health problem in Australia. There are no effective treatments that can reverse or slow these diseases. The research is based on our recent discovery that an enzyme called Hck might play a very important role in lung disease. We used mice in which a genetic method had bee ....This project aims to identify better and safer treatments for serious, life-threatening inflammatory lung diseases, such as Chronic Obstructive Lung Disease (COPD), which affect over 600 million people worldwide and are a major health problem in Australia. There are no effective treatments that can reverse or slow these diseases. The research is based on our recent discovery that an enzyme called Hck might play a very important role in lung disease. We used mice in which a genetic method had been used to change Hck into its active form. The mice appeared normal when they were born but developed a progressive lung inflammation that resembled serious human lung diseases. Surprisingly, the mice also displayed enhanced responses to substances from bacteria that can infect the lung - a so-called innate immune response. This led us to conclude that the main problem in the mice was actually enhanced innate immunity - which is usually protective - turning against the lung to cause disease. To understand exactly what controls this fine balance between protection and lung damage, we will use new and sophisticated gene modification methods that allow us to target changes in Hck activity to specific cells that we suspect are the main cause of the disease. In doing so we will add special tags into these cells, so that we can isolate the controlling molecules in the disease process. We are particularly interested in a cell called the macrophage, a major defensive cell in the lung that is also known to be capable of causing lung disease. Our aim is to find disease-controlling molecules that could be blocked with new drugs that would suppress disease but spare defenses against lung infections.Read moreRead less