Airborne fungi (molds) are ubiquitous saprophytic organisms associated with a spectrum of diseases in immunocompetent individuals, ranging from asthma and allergy to chronic inflammatory lung disease. Molds are emerging pathogens causing necrotizing infections associated with high morbidity and mortality in an expanding group of patients with acquired immune defects. Aspergillus fumigatus is the predominant airborne fungal pathogen in humans and a model pathogen to study phagosome biogenesis and pulmonary host defense. Although severe neutropenia and receipt of corticosteroids are the predominant risk factors for development of invasive mold pneumonia the immunopathogenesis of these infections remains obscure. Therefore, understanding cellular and molecular determinants of host-fungal interaction that are critical for disease pathogenesis is a research priority for development of novel therapies and improve the outcome of these lethal infections.
Our lab is interested in exploring novel immune effector pathways regulating elimination of fungal conidia inside the phagosome of professional phagocytes. In parallel, our research priority is to get mechanistic insight on novel virulent mechanisms employed by airborne fungi to avoid killing by innate host responses. In the long run, we aim to utilize airborne fungi as model pathogens to identify novel signaling pathways with broad physiological role in development of human diseases beyond fungal infections. In order to dissect the complexity of host-fungal interplay our group utilizes genetic approaches in murine and human immune cells and animal models of fungal diseases, including transgenic mice and Drosophila melanogaster fruit flies.
Georgios Chamilos, MD