> *Dissertation Defense Announcement
> To:  The George Mason University Community*
>
> *Candidate: Jessica Helene Chertow
> Program:    PhD Biosciences
> *
> *Date:   Monday May 9, 2011
> Time:   10:00 a.m. 
> Place:  George Mason University
> ** 	     Discovery Hall Auditorium
> 	     Prince William campus <http://www.gmu.edu/resources/visitors/findex.html>
>   
> Dissertation Chair: Dr. Serguei Popov
> Dissertation Director: Dr. Myung Chung
> Committee members: Dr. Charles L. Bailey, Dr. Terry Creque, Dr. Barney Bishop*
> *Title: **"/Bacillus Anthracis/ Protease Regulates Bacterial Adhesion and Invasion"* 
> ****
> The dissertation is on reserve in the Johnson Center Library, Fairfax campus.
> The doctoral project will not be read at the meeting, but should be read in advance. 
> /**/
> *All members of the George Mason University community are invited to attend.*
>
>
> *ABSTRACT: 
> *
>   
> To initiate an efficient bacterial infection, microbes require the binding and in some cases invasion into host cells. To date, BslA, an S-layer prtoein has been identified as a Bacillus anthracis adhesin.  Here, we investigated the role of immune inhibitor A metalloprotease (InhA) of B. anthracis in adhesion and invasion in endothelial cells. We determined that InhA can serve as a negative regulator of adhesion and invasion in human brain endothelial cells (hBMECs) using wildtype Sterne and inhA-deficient (&#916;inhA) bacilli. The complemention of inhA into mutants induced a similar level of binding as wildtype. BslA levels in S-layer extracts of &#916;inhA strain were significantly higher than wildtype and complemented strains. An inverse correlation between InhA and BslA expression was observed when bacilli were cultured in air or bicarbonate/CO2 conditions. Furthermore, BslA was sensitive to purified InhA degradation in a concentration- and time-dependent manner and transcriptional changes in the BslA gene was not observed. Invaded wildtype bacilli were resistant to intracellular killing compared to &#916;inhA strain. Finally, we found InhA serves an important factor to anthrax virulence in late stage disease in mice.  Taken together, these results suggest InhA regulates B. anthracis adhesion by modifying cell surface properties through direct proteolysis of adhesin protein, BslA and bacteria expressing an hyperadhesive phenotype exhibit decreased virulence in mice.
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