"Throughout my search for a graduate program, the Microbiology and Immunology Department of Wake Forest remained at the top of my list.  I was looking for a department with an excellent publication record, solid funding, and a focus on training graduate students to become highly skilled and competitive researchers.  The smaller class size of this department allows for the individualized attention I was looking for, and the wide range of research provides many opportunities for collaboration between immunologists, bacteriologists, and virologists.  In addition to this, the completion of formal coursework within the first year allows students to focus their efforts on research and publication.  Choosing the Microbiology and Immunology Department at Wake Forest was an easy decision, and the dedication of the faculty to the progress of their students continues to impress me."

Effects of AI-2 Quorum Signaling on Haemophilus Influenzae Biofilm

Nontypeable Haemophilus influenzae (NTHi) is a common airway commensal and a leading cause of otitis media featuring biofilm. The exact signals involved in biofilm formation and maturation are not well defined, but quorum signaling may play a role in the establishment of this form of bacterial community. Quorum signaling is a means of communication within populations of bacteria, one form of which involves inter-species signaling via the uptake of Autoinducer 2 (AI-2) produced through the action of the LuxS protein. NTHi is known to possess a luxS homolog and produces functional AI-2. In other bacterial species, AI-2 has been implicated in virulence as well as biofilm formation and maturation. Previous work on NTHi biofilms has shown that lipooligosaccharide (LOS) modifications such as phosphorylcholine (PCho) and sialic acid (Neu5Ac) affect biofilm formation as well as persistence. Thus, I will be addressing the hypothesis that AI-2 quorum signaling impacts virulence by altering biofilm formation and maturation, potentially through regulation of biofilm-promoting LOS modifications. Our data show that NTHi luxS mutants are comparable to wild type in their ability to produce biofilms in vivo. However, the course of infection for luxS mutants differs significantly from wild type in bacterial counts and severity of disease. In addition, luxS mutants were shown by whole-cell ELISA to have reduced PCho content as compared to wild type, indicating a role for AI-2 quorum signaling in LOS modification.