Assistant Professor

Assistant Professor, TouroCOM Montana

My research interests explore the reciprocal communication between Staphylococcus aureus (S. aureus) and the host immune system. Ongoing studies explore S. aureus pathogenesis and immune evasion in two distinct contexts: 1) S. aureus as a paradigmatic pathobiont within the respiratory system and 2) S. aureus biofilm contamination on implanted medical devices.

1) S. aureus is frequently trafficked from the anterior nares into the lower respiratory tract; however, primary lung infections by S. aureus are rare. We hypothesize that components of a healthy lung environment suppress S. aureus virulence production. Our data demonstrate that palmitic acid, the predominant free fatty acid within pulmonary surfactant, reduces toxin production and protects primary human leukocytes from toxin-mediated lysis. Furthermore, preliminary data suggest antecedent infections with influenza disrupt pulmonary surfactant production, leading to increased S. aureus toxin production and toxin-mediated host cell damage.

2) Biofilm growth on implanted abiotic surfaces leads to chronic infections that are increasingly recalcitrant to therapeutic interventions. Using a newly developed mouse model of subcutaneous implantation, we characterize early neutrophil recruitment to contaminated implant surfaces and the periimplant tissue. Data suggest that neutrophil recruitment to highly contaminated implants is minimally boosted compared to sterile controls and that early detection of contaminant organisms by neutrophils is likely critical for bacterial clearance and wound healing. Following surgical events, we hypothesize that immune cells polarize to anti-inflammatory phenotypes that prioritize wound repair over bacterial killing.

The anti-inflammatory environment enables low numbers of contaminant organisms to go undetected by the infiltrating immune cells, allowing for a sufficient window to establish biofilm growth and promote mmune tolerance.