Clear dead cells and cure lung fibrosis
Exposure to various inhaled air toxins like cigarette smoke, chemicals, drugs and so on, increase incidence and severity of chronic lung diseases including asthma and idiopathic pulmonary fibrosis (IPF). Progression of lung fibrosis characterized by tissue thickness and stiffness, increases disease severity and mortality. Environmental toxins damage airway epithelial cells and induce cell death. When immune cells don’t clear dead cells in the airways properly, this can cause severe fibrosis.
We hypothesize that by clearing dead cells, immune cells acquire suppressive ability and inhibit the progression of lung fibrosis. Our aim is to determine the mechanism by which airway immune cells acquire a suppressive ability, called ‘tolerance’ after dead cell clearance; and find the molecular target for the treatment of asthma and IPF.
We will investigate whether boosting these immune cells that live in the lung and clear dead cells, can reduce airway inflammation, in mouse models of asthma and pulmonary fibrosis that mimic the human disease. We will test whether these immune cells of the lung acquire protective capacities after engulfing dead cells. Transcriptomic gene analysis by using RNA sequence technology on lung immune cells engulfing dead cells will be performed, in an attempt to identify novel key regulators of airway tolerance.
We believe these regulatory immune cells maintain airway silence at long term and can be used in asthma or IPF therapies in the clinic. Screening novel targets to act on lung immune cells and promote long term tolerance will stop progression on fibrosis.