Kate Wolf, PhD

Research in my lab is focused on investigating various aspects of host-pathogen interactions during infection with the obligate intracellular bacterium, Chlamydia.  

Chlamydia trachomatis is a Gram-negative human pathogen causing a variety of acute as well as chronic diseases. This bacterium infects primarily epithelial cells of mucosal surfaces of the urogenital tract and the human eye. Chlamydia-mediated genital infections represent the leading cause of bacterial sexually transmitted diseases (STDs) in the United States and worldwide. We study the role of chlamydial, surface exposed, polymorphic membrane proteins (Pmps). C. trachomatis contain nine Pmps, A through I. This family of proteins are immunogenic and represent important virulence factors. We utilize chlamydial mutagenesis to identify and characterize the role(s) Pmps may play during chlamydial attachment to, invasion of, intracellular propagation, and generation of new infectious progeny in epithelial host cells. 

In addition, my laboratory investigates the role(s) the respiratory chlamydial pathogen, C. pneumoniae plays during co-infection with respiratory viruses. The human respiratory tract is exposed to a great variety and number of infectious and non-infectious microorganisms. It is up to our innate immune response to either quickly eliminate these invaders or mount an adequate adaptive immune response to efficiently eradicate respiratory pathogens. Many of these microorganisms invade the same target cells within the respiratory tissues. The majority of the adult population are infected during their life time with C. pneumoniae; with reinfection(s) being a common occurrence. During the recent pandemic, caused by the coronavirus SARS-CoV-2, it has been reported from numerous hospitals worldwide that a significant number of patients infected with SARS-CoV-2 suffering from severe disease manifestations were co-infected with C. pneumoniae. We have demonstrated that this obligate intracellular bacterium employs species-specific strategies to impair the anti-viral innate immune response in infected epithelial cells, which may result in a significant enhancement of viral propagation. C. pneumoniae is likely to share the eukaryotic host cell with other, primarily viral pathogens. The bacterium modulates the host cell environment promoting chlamydial pathogenesis and by doing so, impacts other, non-related infectious microorganisms within the infected tissues. We study the effects of modulation of the innate immune response in C. pneumoniae infected epithelial cells on viral survival and propagation.