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Mechanism Of Exacerbations In Cystic Fibrosis Lung Disease
Funder
National Health and Medical Research Council
Funding Amount
$254,876.00
Summary
Cystic Fibrosis lung disease is characterised by infeciton with a bug called Pseudomonas aeruginosa. Patients ultimately die in their mid-30's as a result of this infection, but lung decline is accelerated by episodes of exacerbation when patients cough up large volumes of mucky sputum. We are studying the casue of exacerbations by looking at bacterial behaviour and the response of the immune system. We will use this information to try and develop early warning signals and better treatments.
Identification Of Proteins Specific To Transmissible Pseudomonas Aeruginosa In Cystic Fibrosis Infection
Funder
National Health and Medical Research Council
Funding Amount
$443,007.00
Summary
Cystic fibrosis (CF) is the most common autosomal recessive disorder in humans, affecting 1:2000 people. Mortality is often caused by Pseudomonas aeruginosa lung infections which have recently been shown to occur not only environmentally but also via person-person contact, usually during CF clinic visits. This project will elucidate the molecular traits responsible for these 'epidemic' P. aeruginosa infections, with the aim of finding novel therapeutics and infection control strategies.
The lung in people with the genetic disorder cystic fibrosis (CF) contains increase amounts of iron, which promotes bacterial infection. In this research project we are using mouse models of CF and airway cells obtained from people with CF to investigate the underlying mechanism of abnormal iron regulation. We are also examining the therapeutic potential of compounds that interfere with the ability of bacteria to obtain iron to see whether this can overcome antibiotic resistance.
Bacterial Activation Of Epithelial Barrier Function
Funder
National Health and Medical Research Council
Funding Amount
$341,953.00
Summary
This project deals with a bacterium that is a major cause of hospital-acquired infections and is the main cause of disease for people with cystic fibrosis. The project aims to identify the cell components that are actively involved in signalling a bacterial infection in the lung and how the body adapts to this interaction. This work will allow us to better understand the biology of the lung and how it copes with infection and may lead to the development of new antibiotics.
Genomic Adaptation Of Pseudomonas Aeruginosa In The Cystic Fibrosis Airway
Funder
National Health and Medical Research Council
Funding Amount
$133,351.00
Summary
Pseudomonas aeruginosa (Pa) is an important respiratory pathogen in Cystic Fibrosis (CF) which causes substantial morbidity and mortality. Its genetic versatility enables it to thrive in a wide diversity of environment. This study aims to assess the genomic adaptation of the common Pa strains among the Australian CF patients during chronic infection and during intravenous antibiotics therapy. The study results can lead to development of novel treatment options for Pa infection in CF.
Multi-copper Oxidase Mediated Iron Uptake In Ps. Aeruginosa And Other Pathogenic Bacteria: Mechanism And Role In Disease
Funder
National Health and Medical Research Council
Funding Amount
$73,500.00
Summary
Iron is essential for the growth of bacteria. One of the mechanisms used by humans (and other animals) to defend against bacteria that cause disease is to trap iron by binding it to a set of iron binding proteins eg. transferrin. In this way there is no free iron in the system, so bacteria that survive in humans have had to evolve specific mechanisms to remove the iron form these host proteins. The mechanisms of iron uptake in pathogenic bacteria have been studied extensively, and the iron uptak ....Iron is essential for the growth of bacteria. One of the mechanisms used by humans (and other animals) to defend against bacteria that cause disease is to trap iron by binding it to a set of iron binding proteins eg. transferrin. In this way there is no free iron in the system, so bacteria that survive in humans have had to evolve specific mechanisms to remove the iron form these host proteins. The mechanisms of iron uptake in pathogenic bacteria have been studied extensively, and the iron uptake systems are considered to be important of virulence factors (bacterial factors essential for causing disease). Humans and other higher organisms like Yeast have an iron uptake system that uses multi copper oxidase proteins (MCOs). These proteins have a ferroxidase activity, which converts iron from a protein bound insoluable form Fe (III) to a soluble form Fe(II), allowing it to be released from iron binding proteins. We have searched the genomes of many bacteria for a similar system and have discovered that many bacteria have MCOs. We wanted to test the idea that the bacteria MCOs we have identified may be involved in iron uptkae. If so, it would represent a huge step forward in understanding this important process and could lead to products for prevention or better treatment of infectious disease. We chose the disease causing bacterium Pseudomonas aeruginosa for our study. We have shown that the MCO has ferroxidase activity (Fe(III)>Fe(II), we have made a mutation in the MCO gene had have shown that the bacterium lacking MCO will not grow under certain conditions. These conditions are consistent with a defect in iron uptake. We have identified but not characterised several other key compnents of this iron uptake system. In the proposed work we wish to investigate all of the components of this iron uptake system in this important pathogen, and to initiate studies in other bacteria pathogens.Read moreRead less
Molecular Characterization Of The Role Of FtsK In Chromosome Unlinking And Segregation.
Funder
National Health and Medical Research Council
Funding Amount
$471,022.00
Summary
Bacterial pathogens, especially those associated with multiple drug resistances, are becoming increasingly serious health problems. This project will investigate the key protein FtsK and the role it plays in co-ordinating bacterial chromosome segregation and cell division. FtsK from three specific pathogens, Escherichia coli, Pseudomonas aeruginosa and Staphylococcus aureus, will be characterized to better understand its vital role, and to inform and focus future drug design.