Candida species are the most common opportunistic fungal
pathogen, causing both mucosal infection and invasive disease. Recently,
alarming increases in strains resistant to antifungals, including the
most frequently isolated C. albicans and the emerging multi-drug resistant C. auris,
led the CDC to classify anti-fungal resistant fungal species as a
serious threat. When antifungal treatment fails, patient outcome is
determined by the balance between productive infection control and
effective limitation of damaging host responses. In our research, we
study how both host and fungal factors contribute to immune
dysregulation and damage in the context of Candida infection,
leveraging this knowledge for the development of novel and effective
therapeutic strategies. Since these fungi are a common yet
underappreciated member of the human microbiota, we also seek to
understand how fungal colonization and virulence may modulate
polymicrobial infection as well as contribute to the pathogenesis of
chronic inflammatory and autoimmune disorders. By employing a mixture of
mouse models and cell culture systems to investigate fungal
interactions with the host and with other microbes, we test the
hypothesis that disease severity and host susceptibility to fungal
infection can be ameliorated by appropriate targeting of detrimental
host immunity. Current areas of focus include 1) Candida
modulation of the host and microbial response during urinary tract
infection, 2) antimicrobial peptide regulation of inflammation during
fungal sepsis and 3) impact of underlying immune disorders on the host
response to fungal infection.