The current goals of my research are to better understand lung immune responses during acute vs. chronic exposure to the opportunistic fungal pathogen Aspergillus fumigatus. During acute exposure, which is an infection model mimicking invasive pulmonary aspergillosis, 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 my laboratory over the last several years has been focused 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.