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Matthew A. Mulvey

Associate Professor of Pathology

B.S. University of Texas, Austin

Ph.D. University of Texas, Austin

Research

References

mulvey@path.utah.edu

Matt Mulvey's Lab Page

Matt Mulvey's PubMed Literature Search

Research

My lab is focused on understanding the survival and virulence strategies employed by a group of important bacterial pathogens collectively known as Extraintestinal Pathogenic Escherichia coli, or ExPEC. These bacteria can persist within the human gut, often without apparent pathological consequence, but have the capacity to disseminate and cause disease in other host niches, including the blood, central nervous system, and the urinary tract. Subsets of ExPEC known as Uropathogenic E. coli (UPEC) are the primary cause of urinary tract infections (UTIs), which currently rank among the most common of infectious diseases worldwide. These bacteria act as opportunistic invasive pathogens capable of entering host epithelial cells within the urinary tract where they can either rapidly multiply or alternatively persist in a more quiescent state for days to many weeks. We, and others, hypothesize that intracellular reservoirs of UPEC may contribute to the often chronic and recurrent nature of UTIs. ExPEC strains related to UPEC can have a broad host range and display a remarkable ability to adapt to widely varying environmental conditions, often facing nutrient limitations, antibiotics, and aggressive host defense mechanisms. Using genetics, microscopy, biochemistry, global gene expression analysis and molecular biology techniques coupled with cell culture, mouse, and zebrafish infection model systems, we are working to delineate both bacterial and host factors that control the ability of ExPEC to colonize and persist within the host. Specific goals of this research include:

1. Defining the mechanisms by which ExPEC invades, traffics, multiplies, and persists within host cells and tissues
2. Understanding how small regulatory RNAs and other bacterial factors modulate ExPEC virulence gene expression and, ultimately, bacterial resistance to the multitude of stresses encountered during the course of an infection.
3. Determining how ExPEC-associated toxins and other virulence factors modulate and hijack host signaling events, including host cell death, survival, and inflammatory pathways

 

Figure: Model depicting key events involved in host cell invasion, intracellular trafficking, persistence, growth, and eventual efflux of UPEC.

References