Targeting linear ubiquitination to attenuate inflammation and promote repair after IAV infection

Recovery from severe influenza is a clinically important yet understudied process. A central hypothesis of this project is that the persistence of respiratory failure and the development of multiple organ dysfunction in patients with pneumonia/ARDS is a consequence of the failure of normal mechanisms of inflammation resolution and lung tissue repair. We propose to investigate the process of recovery from viral pneumonia with a focus on how the dysregulated production of inflammatory mediators from the lung epithelium prevents epithelial regeneration by inhibiting the reparative function of monocyte-derived alveolar macrophages.