Here in the Steele Lab, our current projects relate to the understanding of the pulmonary immune responses, both acute and chronic, to the opportunistic fungal pathogen Aspergillus fumigatus. Our acute model mimics the pathology observed in invasive pulmonary aspergillosis and our major focus is on the cytokine IL-22. Specifically, we investigate pathways that positively and negatively regulate IL-22 production as well as the antifungal immune pathways induced by IL-22. Themes in this area of investigation include common γ-chain cytokines, innate lymphocytes, and eicosanoid biology.
An important shift in the lab over the last several years has been an emphasis on the identification of inflammatory biomarkers, immune cells and pathways in human lung diseases that correlate with functional decline, and bringing these observations back to experimental animal models to provide mechanistic insight (i.e. bedside-to-bench). To this end, during chronic exposure, which is a model of severe asthma with fungal sensitization as well as chronic fungal exposure during diseases such as cystic fibrosis, our major focus is on various inflammatory mediators we have identified in human subjects. Themes in this area of investigation include various IL-1 family members, unique chemokines and chitinases/chitinase-like proteins.