Elie El Agha was born in Saida, Lebanon. For his Master thesis, he received a fellowship to work in the lab of Prof. For his early career achievements, he was awarded two start-up grants and one intramural fund in addition to other prizes and awards. The El Agha lab focuses on the cellular and molecular mechanisms mediating lung development and repair, particularly the interaction between mesenchymal niche cells and their epithelial partners along the proximo-distal axis in the respiratory tree.
The lab is interested in the involvement of developmental signaling mechanisms in disease progression versus resolution, especially in the context of pathogen-induced lung injury. Lung injury resulting from bacterial or viral infections represents a serious threat to global health. For instance, influenza A virus and coronavirus outbreaks can lead to pandemics resulting in millions of deaths worldwide.
The latter is defined by the acute onset of noncardiogenic pulmonary edema, hypoxemia and the need for mechanical ventilation. Among the prominent features of ARDS are diffuse alveolar damage and collagen deposition. Pathogen-induced lung diseases are associated with a high socio-economic burden and they mostly lack preventive or curative therapy.
In this context, available therapeutic options for affected patients are predominantly supportive and are incapable of efficiently inducing regeneration in damaged lungs. Importantly, pathogen-induced pneumonia per se not only leads to acute life-threatening conditions such as ARDS but also 1 acts as a secondary hit that contributes to the initiation of fatal and progressive lung diseases such as idiopathic pulmonary fibrosis IPF and 2 represents a comorbidity that contributes to exacerbations such as in chronic obstructive pulmonary disease COPD and IPF.
Thus, acute exacerbations and hospitalization due to pathogen-induced lung injury represent an increased risk in patients with chronic lung disease. Therefore, better understanding of the cellular and molecular cues that mediate pathogen-induced lung injury and the associated repair mechanisms is an urgent clinical need. In this regard, there is a general consensus that developmental processes of lung morphogenesis are recapitulated or at least mimicked in lung repair during adult life.
