Research in the Hogaboam Laboratory addresses two major themes related to chronic pulmonary disease.
The first encompasses the cellular and molecular immune mechanisms that regulate the pulmonary growth and persistence of fungal (summarized in Figure 1) and viral signals in a number of experimental murine models of allergy, hypersensitivity and asthma. Our data to date has revealed that key immune cells such as myeloid cell progenitors, macrophages and dendritic cells bridge the pulmonary innate and adaptive immune responses to these signals. We are presently pursuing several therapeutic interventions with industry collaborators.
Second, and more translational, we explore a grouping of clinical diseases collectively known as idiopathic interstitial pneumonias (IIPs). IIPs are characterized by a lethal fibrotic response due to an exuberant fibroproliferative response by collagen-producing cells in the lung. The mechanism leading to aberrant fibroproliferation in these diseases is an active area of investigation, and we are presently testing the hypothesis that a "misguided" innate immune response is a major cause for destructive fibrotic responses (Figure 2). Using human lung diagnostic biopsy tissues and isolated human cell populations (e.g., stromal and stem/progenitor-like), the Hogaboam Lab is using large-scale genomic, proteomic and novel animal model approaches to explore the etiopathogenesis of these diseases and, more importantly, identify novel therapeutic targets in IIPs.