Annual Report 2020
Project Title: The impact of regulatory cytokines on lung repair during influenza infection
Influenza affects 5-10% of people in Scotland each year, and the disease kills in multiple ways. The virus hijacks the cells of our lungs, turning them into factories for new virus production and preventing their normal operation as the cells we need to breathe. Our bodies’ defence system, the immune system, spings into action and releases an arsenal of molecular weapons to destroy the virus, and in doing so destroys many lung cells too. Current treatment strategies use either anti-virals, aiming to reduce the damage caused by the virus, or vaccines, trying to fine-tune our immune responses to make them more effective and reduce collateral damage.
Our project aims to develop a third approach: we want to harness the lung’s repair process to restore normal lung function as quickly and as effectively as possible. We are focussing on stem cells deep in the lung that fuel lung repair, and we are aiming to identify the signals that activate these cells and determine whether they generate new, healthy lung tissue or harmful scar tissues. We think that signals from the immune system could be a decisive factor in the action of these repair stem cells. So far, we have identified the factor IL-10 as an immune signal with the potential to promote lung stem cell proliferation and lung tissue repair. We are now working out how IL-10 achieves these effects, directly or indirectly, and testing whether manipulating the availability of IL-10 can influence the quantity and quality of lung repair during influenza virus infection.
We hope that by demonstrating the proof of concept, that immune signals can be manipulated to optimise the lung repair process, we can open up a new therapeutic strategy that could promote lung repair and reduce the severity of disease during influenza.
Awarded: Research Incentive Grant
Field: Microbiology, Immunology & Developmental Biology
University: University of Glasgow