Immune-mediated control of epithelial integrity: Does the immune response to influenza infection cause long-term changes in lung function?

Studentship strategic priority area:Basic Bioscience Underpinning Heath
Keywords:Lung, influenza, immunity, cytokines, repair

Abstract:

Influenza virus infection causes extensive lung damage, caused both by the virus and by the immune response. Surviving influenza requires a careful balance between factors that promote immunity and eradicate the virus, and factors that limit the immune response and minimise collateral damage to the lung. One way to limit damage and reduce disease is to drive an active process of repair and regeneration in the lung, and specifically in the airway epithelium - the cells that line the airways and provide the essential gas exchange as we breathe. In this project we will examine which signalling molecules of the immune system are released into the lung during the immune response to influenza virus infection, and how these signals affect epithelial repair and regeneration durign and after infection. We hypothesise that immune signals are essential to maintain barrier integrity in the lung and to enable gas exchange to continue. Previous evidence suggests that repaired epithelium, after infection, is different to the original epithelium, and we suspect that these changes may contribute to multiple pulmonary disorders including secondary infections, increased sensitisation to allergens, and long-term fibrosis. Our aim is to investigate the role of regulatory immune signals in directing the process of epithelial repair during influenza virus infection, and in the long-term consequences.