> Thesis Defense Announcement
> To:  The George Mason University Community
>
> *Candidate: Steve St. John
> Program: Master of Science in Biology
> *
> *Date:   Tuesday April 16, 2013
> Time:   10:00 a.m.
> Place:  George Mason University, 
> 	    Prince William Campus <http://www.gmu.edu/resources/welcome/Directions-to-GMU.html>
> 	    Bull Run Hall, Room 253
> *
>   
> *Title: *"Bacillus anthracis Co-Opts Nitric Oxide and Host Serum Albumin for Pathogenicity in Hypoxic Conditions"**
>
> *Thesis Director*: *Dr. Serguei Popov***
>
> *Thesis Committee*:  *Dr. Daniel N. Cox and Dr. Geraldine Grant
> *A copy of the thesis will be available in the Johnson Center 
> Library.  All are invited to attend the defense.
>
> *ABSTRACT *
> Bacillus anthracis is a dangerous pathogen of humans and many animal 
> species. Its virulence has been mainly attributed to the production of 
> Lethal and Edema toxins as well as the antiphagocytic capsule. Recent 
> data indicate that the nitric oxide (NO) synthase (baNOS) plays an 
> important pathogenic role at the early stage of disease by protecting 
> bacteria from the host reactive species and S-nytrosylating the 
> mitochondrial proteins in macrophages. Another toxin-independent 
> mechanism relevant to late-stage anthrax was shown with non-phagocytic 
> host cells exposed to pathogenic factors secreted by B. anthracis in 
> microaerobic (hypoxic) conditions. In addition to synergistic effect 
> of the pore-forming hemolysin (anthrolysin O) perforating the host 
> cell and the fermentation metabolite (succinic acid) fueling the 
> release of reactive oxygen species from mitochondria, this mechanism 
> involves the activity of NO-derived toxic product(s). In this study we 
> for the first time present evidence that NO produced by baNOS 
> participates in the generation of highly reactive oxidizing species 
> which could be abolished by the NOS inhibitor L-NAME, free thiols, and 
> superoxide dismutase but not catalase. The formation of toxicants is a 
> result of the simultaneous formation of NO and superoxide leading to a 
> labile peroxynitrite and its stable decomposition product, nitrogen 
> dioxide. The toxicity of bacteria could be potentiated in the presence 
> of bovine serum albumin, which serves as a trap of a volatile NO 
> accelerating its reactions. Our data suggest that during infection in 
> the hypoxic environment of pre-mortal host the accumulated NO is 
> expected to have a broad toxic impact on host cell functions.
>
>
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