Assistant Professor of Microbiology and Immunology
Dr. McBride joined the Emory faculty in June 2012. She received her Ph.D. degree from the University of Texas Health Science Center at San Antonio in 2005 and her Bachelor of Science degree from McNeese State University in 1999. She trained as a postdoctoral fellow in the field of bacterial pathogenesis at the Schepens Eye Research Institute of Harvard Medical School from 2005 to 2008 and at the Tufts University School of Medicine from 2008 to 2012. Dr. McBride’s research will focus on identifying the molecular mechanisms of the gastrointestinal pathogen Clostridium difficile that allow it to live within the host. Her work has identified novel mechanisms used by this bacterium to resist killing by antimicrobial peptides, for which she has received an NIH Mentored Research Scientist Development Award. Her work has been published in the Journal of Bacteriology, Microbiology, Infection and Immunity, Molecular Microbiology and PLoS One.
Research in our laboratory centers on the emerging pathogen, Clostridium difficile. C. difficile causes chronic intestinal disease that is both difficult and costly to treat. To colonize the intestine and cause persistent disease, the bacterium must be able to circumvent killing by host innate immune mechanisms. The production of cationic antimicrobial peptides (CAMPs) by the innate immune system represents a critical component of host defense against infections that bacteria must overcome to cause persistent disease. Resistance to these peptides is a demonstrated virulence factor for many bacterial pathogens. We hypothesize that resistance of C. difficile to antimicrobial peptides plays a major role in the ability of the bacterium to colonize the human intestine and cause disease. As such, our laboratory is focused on identifying and understanding the mechanisms that C. difficile utilizes to resist CAMPs produced by the host and the indigenous microbiota of the intestine. To date, we have identified multiple CAMP resistance mechanisms employed by C. difficile, including the novel bacteriocin resistance mechanism, CprABC. By uncovering the bacterial resistance mechanisms that influence disease progression, it is expected that this research will generate knowledge that can be used to manipulate the interactions between the bacteria and the host to prevent and treat infections.