The Role Of MicroRNAs As New Anti-inflammatory Targets For The Treatment Of Asthma
Funder
National Health and Medical Research Council
Funding Amount
$625,655.00
Summary
Asthma is a significant health and economic burden to our society and its prevalence has increased over the last 25 years. New ways of treating asthma are urgently required as current therapeutics treat the symptoms and not the cause of the disease. Asthma is widely thought to be due to the abnormal accumulation of white blood cells (inflammation) in the lungs of diseased individuals. In this project we are exploring new advanced ways to inhibit inflammation and the development of disease.
Galectin-3 And Phagocyte Function In Severe Asthma
Funder
National Health and Medical Research Council
Funding Amount
$698,084.00
Summary
Asthma, a major chronic inflammatory disease affects more than 2 million Australians. Neutrophilic severe asthma is not responsive to current therapies. We have recently made a significant advance in understanding neutrophilic asthma, reporting low levels of a protein called galectin-3 (gal-3). In this project we will explore the role of gal-3 its effect on the resolution of inflammation. This study will result significantly advance the knowledge of the mechanisms of neutrophilic severe asthma.
Therapeutic Potential Of The IL-3-IL-5-GM-CSF Common Beta Receptor To Treat Upper And Lower Allergic Airway
Funder
National Health and Medical Research Council
Funding Amount
$150,442.00
Summary
This research aims to develop new treatments for allergic diseases such as asthma and allergic rhinitis, which remain significant public health problems in Australia. We will develop new therapies with the potential to completely suppress acute and chronic allergic disease targeting a common receptor protein that controls multiple facets of allergic inflammation. We will test antibodies intended to treat human asthma using a novel mouse strain expressing the human form of this receptor.
Role Of IL-3 In Allergic Inflammation: Modulation Of Basophils, Mast Cells, Eosinophils And Remodelling In Asthma.
Funder
National Health and Medical Research Council
Funding Amount
$495,380.00
Summary
Asthma is an important disease in the Australian community. We will investigate how the underlying inflammation in this disease is controlled and will focus our studies on a hormone-like regulator of the immune system called interleukin-3. Our hypothesis is that interleukin-3 regulates basophils, mast cells and remodelling of the airways which are central features of asthma. This study will give a better understanding of how the inflammation is caused and information for new drug targets.
The Role Of MicroRNAs In The Regulation Of Antiviral And Inflammatory Responses During Experimental Rhinovirus Infection
Funder
National Health and Medical Research Council
Funding Amount
$605,096.00
Summary
Asthma exacerbations due to viral infections are a major health and economic burden to our society. Treatment of asthma exacerbations focuses on reducing the symptoms rather than the cause of the disease. Virus-induced asthma exacerbation are widely thought to be due to an abnormal influx of white blood cells into the lungs (inflammation) and an altered anti-viral responses. In this project we will explore novel strategies to inhibit inflammation and to promote the anti-viral response.
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
I am a physiologist-pharmacologist examining fundamental mechanisms of chronic inflammatory disease. By defining these mechanisms, I seek to discover the underlying cause of disease and to identify novel strategies for diagnosis and therapy of chronic diseases that are worldwide causes of morbidity and mortality.
Regulation Of Extrinsic Death Pathways In Neutrophils
Funder
National Health and Medical Research Council
Funding Amount
$84,656.00
Summary
During infection, the lifespan of neutrophils normally increases despite an abundance of neutrophil death signals in inflamed tissues. Altered lifespan of neutrophils has been reported in diseases associated with influenza, Streptococcus, RSV and cytomegalovirus infection. Our research has discovered a relationship between the two dominant death pathways in neutrophils, indicating that alterations in one death pathway protect the neutrophil from death signals from the second death pathway.