Jonathon P. Audia, Ph.D.

Associate Professor
Phone: (251) 460-6929
FAX: (251) 460-7931


Physiology and Gene Regulation of Rickettsia

Microbial Physiology and Host Pathogen Interactions

Dr. Jonathon P. Audia, Associate Professor, received his Baccalaureate and Masters Degrees in Science from McMaster University in Hamilton, Ontario, Canada, and his Ph.D. in Basic Medical Sciences from the University of South Alabama College of Medicine.

My lab studies the obligate intracellular pathogen, Rickettsia prowazekii - a category B priority pathogen and a Select Agent.  Rickettsiae are transmitted by arthropods and cause human diseases such as epidemic typhus and Rocky Mountain spotted fever.  As obligate intracellular pathogens, these fascinating organisms grow exclusively in the cytoplasm of the host cell, unbound by any host cell-derived membrane structures.  The goal of my research program is to further our understanding of the mechanisms evolved by rickettsial pathogens to parasitize eukaryotic host cell cytosol as its sole growth niche and cause disease.  Our major areas of interest include:

The Role of Phospholipases in Mediating Host-Pathogen Interactions:

Phospholipases (PLs) are enzymes that hydrolyze phospholipids and are emerging as important elicitors of second messengers that affect cellular processes involved in modulation of innate immune cell function and inflammation.  We are working to understand the roles of phospholipase A (PLA) and phospholipase D (PLD) enzymes in R. prowazekii infection of microvascular endothelial cells and macrophages using a combination of biochemical and cell biology approaches.  These studies will ultimately allow us to determine if selective inhibition of rickettsial PLs is a viable strategy to limit infectivity.

Transport Physiology and the Evolution of Obligate Intracellular Parasitism

Obligate intracytoplasmic growth has had profound effects on the evolution of rickettsial physiology.  Imagine growing in nutrient rich cytoplasm, bathed by precursors, intermediates, and end products of cellular metabolism - as a consequence, it appears as if the rickettsia has abandoned many of its own de novo biosynthetic pathways in favour of acquiring metabolites directly from the host cell cytoplasm.  Our goal is to discover novel rickettsial transport systems that allow the pathogen to parasitize nutrients available in host cell cytosol using biochemical approaches.  Because these transport systems are rarely, if ever, found in free-living bacteria or the eukaryotic host cell they are attractive as potential targets for therapeutic discovery.


Recent Publications

Click here for a list of recent publications.



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