Focus areas
In Dr. Jerschow's lab, we are advancing understanding of aspiring-exacerbated respiratory disease (AERD) and related conditions through the following research:
- The immune mechanism of AERD and chronic rhinosinusitis with nasal polyps. We focus on the role of type 2 immunity in AERD, which is linked to severe eosinophilic asthmatic symptoms that are complicated by recalcitrant chronic sinusitis with nasal polyposis. The goals of this research are to better understand the pathophysiologic mechanism and develop better medical treatments for patients with chronic allergic conditions.
- Mast cell responses to nonsteroidal anti-inflammatory drugs (NSAIDs). Typical features of AERD include increased numbers of mast cells and activation of these cells, along with the systemic NSAID-induced release of multiple mediators. We are studying the role of mast cells in the mechanism of aspirin intolerance, emphasizing the release of cytokines and eicosanoids. We compare transcriptomic, epigenomic and metabolomic profiles of mast cells from people who are sensitive to and tolerant of aspirin.
- Staphylococcal serine proteases in type 2 inflammation. Staphylococcus aureus, an opportunistic pathogen, is associated with nasal polyps in patients with chronic rhinosinusitis and AERD. We are using biochemical and molecular biology approaches to investigate how staphylococcus can orchestrate immune background through secretion serine protease.
- Comparative genomics of Staphylococcus aureus. Studies show that murine models respond differently to staphylococcus that has been isolated from patients with and without nasal polyps. We are examining the genomic heterogeneity of staphylococcus to understand the spectra of bacterial metabolism, ecology and virulence.
- The function of prostaglandin D2 (PGD2) in AERD. AERD is associated with overproduction of PGD2, and the biological effects of PGD2 are mediated by DP1 and CRTH2 receptors. Our research investigates the function of PGD2 in AERD using in vitro and ex vivo models.