Role of the Small GTPase RhoG in Neutrophil Activation

Abstracts are not currently available in GtR for all funded research. This is normally because the abstract was not required at the time of proposal submission, but may be because it included sensitive information such as personal details.

When our lungs are invaded by viruses and bacteria, our immune system sends white blood cells to the site, which 'eat' and destroy the invaders. Unfortunately, the weapons that white blood cells use to kill bacteria can sometimes also damage our own lung tissue. This damage can cause diseases like Acute Respiratory Distress Syndrome (ARDS) and Bronchiectasis. At the moment, this process is not well understood and we have no strategies for preventing it. We have been studying a protein in the lungs, known as a small GTPase. We have genetic evidence that this protein has an important role in cells that are a major cause of ARDS. Mice that don't have the protein are perfectly able to fight infections from things like bacteria, but do not experience any associated lung damage. This suggests that this protein is involved in the process that damages lung tissue. This research aims to understand how our immune system attacks the lungs in this way. In so doing the researchers will make advances to prevent such damage. This grant from The British Lung Foundation is to determine whether this signalling mediator is potentially a good target for drugs to fight ARDS. Anti-inflammatory drugs available to treat lung disease are currently very non-specific, affecting many cell types and usually preventing the beneficial effects of white cells in fighting infection. Such drugs (e.g. corticosteroids) thus have many side effects including increased susceptibility to infection. By finding and understanding a new signaling pathway, we hope to identify possible drug targets that may limit inflammation without leading to increased risk of infection. This research may thus lead to novel treatments for ARDS and other inflammatory lung diseases.

unavailable