Pennsylvania State University, BS, 2005
University of Maryland—Baltimore, PhD, 2010
Dr. Brian Peters received his Bachelor of Science in Microbiology from the Pennsylvania State University in 2005. He then received his PhD from the University of Maryland—Baltimore in 2010, where he studied bacterial-fungal biofilm-mediated interactions in the laboratory of Dr. Mark Shirtliff. Dr. Peters then trained as a postdoctoral fellow in the lab of Dr. Mairi Noverr in the Dept. of Oral Biology at LSUHSC, where he further explored polymicrobial interactions in the context of host innate immunity. Currently, Dr. Peters continues to study innate immunity with special emphasis on polymicrobial disease as an Assistant Professor – Research in the Noverr lab.
Dr. Peters’ current research interests focus on using the ubiquitous bacterial pathogen Staphylococcus aureus and the opportunistic fungus Candida albicans as model organisms for studying the pathogenesis of polymicrobial disease. Although microbes are commonly found living as complex consortia in the environment and on the human host, relatively little is known about how microbes interact and the consequences of these interactions on human health and disease. Therefore, the overall goal of Dr. Peters’ research is to elucidate the mechanisms by which microbes can synergize their virulence resulting in augmented disease.
Our lab currently uses a mouse model of polymicrobial peritonitis to study C. albicans-S. aureus interactions in vivo. Monomicrobial infections with either C. albicans or S. aureus alone are non-lethal. However, co-infections with these same doses result in rapid mortality. Our lab has identified that the immunomodulatory oxylipin, prostaglandin E2 (PGE2) plays a major role in mediating mortality in co-infected mice. Pharmacologic intervention with the cyclooxygenase inhibitor indomethacin protects mice from lethal peritonitis, and may provide insight into potential novel therapies for peritoneal infections. Current experiments seek to elucidate the role of staphylococcal toxin secretion and oxylipin signaling during polymicrobial disease.
An exciting new project in our lab focuses on the host innate signaling mechanisms resulting in the hallmark PMN response during Candida vaginitis. In collaboration with the Fidel lab, we are interested in exploring inflammasome function during Candida vaginitis and modulation of this pathway as a novel immunotherapeutic approach against such infections. Ongoing studies aim to define the role of morphogenesis and associated fungal virulence factors involved in this immunopathological response. Further research seeks to expand these findings to polymicrobial models of disease.
Candida albicans, Staphylococcus aureus, biofilm, polymicrobial, vaginitis, inflammasome, prostaglandin
School of Dentistry: Methods in Research, Dental Rounds
Peters BM, Yano J, Noverr MC, Fidel PL Jr. Candida vaginitis: when opportunism knocks, the host responds. PLoS Pathogens. In press, 2014.
Yano J, Palmer GE, Eberle KE, Peters BM, Vogl T, McKenzie AN, Fidel PL Jr. Vaginal epithelial cell-derived S100 alarmins induced by C. albicans via pattern recognition receptor interactions is sufficient but not necessary for the acute neutrophil response during experimental vaginal candidiasis. Infect Immun. 2014 Feb;82(2):783-92.
Peters BM, Palmer GE, Nash AK, Lilly EA, Fidel PL Jr, Noverr MC. Fungal morphogenetic pathways are required for the hallmark inflammatory response during Candida vaginitis. Infect Immun. 2014 Feb;82(2)532-43.
Peters BM and Noverr MC. Candida albicans-Staphylococcus aureus polymicrobial peritonitis modulates host innate immunity. Infect Immun. 2013 Jun;81(6):2178-89. PMCID: PMC3676024.
Peters BM, Ward RM, Rane HS, Lee SA, Noverr MC. Efficacy of ethanol against Candida albicans and Staphylococcus aureus polymicrobial biofilms. Antimicrob Agents Chemother. 2013 Jan;57(1):74-82. PMCID: PMC3535989.
Peters BM, Jabra-Rizk MA, Hoyer LL, Krom BP, Meijering R, Shirtliff ME. Cross-Kingdom polymicrobial biofilm communities: S. aureus adherence to C. albicans hyphae is mediated by the hyphal adhesin Als3p. Microbiology. 2012 Dec;158(Pt 12):2975-86.
Peters BM, O’May GA, Jabra-Rizk MA, Costerton JW, Shirtliff ME. Polymicrobial interactions: impact on pathogenesis and human disease. Clin Microbiol Rev. Jan;25(1):192-213, 2012: PMCID: PMC3255964.
Peters BM, Jabra-Rizk MA, Leid JG, Costerton JW, Shirtliff ME. Microbial interactions and differential protein expression within Candida albicans-Staphylococcus aureus polymicrobial biofilms. FEMS Immunol Med Microbiol. Aug:59(3):493-503, 2010. PMCID: PMC2936118.
Peters BM, Zhu J, Scheper MA, Hackett W, Al Shaye S, Fidel Jr., PL, Jabra-Rizk MA. Efficacy of histatin-5 against Candida albicans in an ex vivo murine model of oral infection. FEMS Yeast Res. Aug:10(5):597-604. PMCID: PMC2921938.