Alison Coady, PhD
Assistant Professor
Department of Microbiology & Immunology
Office: MRB 3.142G
Lab: MRB 3.164/3.166
Email: alcoady@utmb.edu
Education |
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Postdoctoral Fellowship University of California San Diego | April 2022 San Diego, CA |
PhD, Biomedical Sciences University of California San Diego | December 2014 San Diego, CA |
BS, Microbiology, minor in Chemistry University of Washington | June 2003 Seattle, WA |
Research Interests |
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Fungal pathogenesis and immunology, bacterial-fungal interaction, sepsis, urogenital infection, antimicrobial resistance |
Current Research |
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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. |