Brian M Peters, PhD

Assistant Professor
Department of Clinical Pharmacy

Office: 341 COLLEGE OF PHARMACY BUILDING
881 MADISON AVENUE
MEMPHIS TN 381632198
Tel: (901) 448-2724
bpeter21@uthsc.edu

Education

  • PostDoc, Louisiana State Health Sciences Center. New Orleans, LA., Fungal pathogenesis
  • Ph.D., University of Maryland--Baltimore. Baltimore, MD., Molecular Microbiology and Immunology
  • B.S., Penn State University. University Park, PA., Microbiology

Research Description

The Peters lab has two main foci of research: 1) the host and fungal molecular mechanisms responsible for the immunopathogenesis of vulvovaginal candidiasis and 2) quorum sensing and toxin regulation during fungal-bacterial intra-abdominal infection. 

Immunopathogenesis of vulvovaginal candidiasis:

Candida albicans, an opportunistic human fungal pathogen, is the leading causative agent of vulvovaginal candidiasis (VVC) and presents major quality of life issues for women worldwide. It is estimated that nearly every woman of childbearing age will be afflicted by VVC at least once in her lifetime. Aside from periodic infections, 5-10% of all women suffer from recurrent VVC (RVVC), resulting in chronic episodes of vaginal irritation and pain, requiring antifungal maintenance therapy to partially control symptoms. Although these treatments are typically effective at reducing organism burden, static function of azole activity, fungal recalcitrance to clearance, and lack of comprehensive understanding of disease pathology necessitates further insight into the host and fungal factors that contribute to vaginitis immunopathology.

We are interested in exploring virulence mechanisms utilized by C. albicans to activate the inflammasome at the vaginal mucosa and determining the downstream signaling events relevant to disease pathogenesis. Exploitation of this this pathway may be used as a novel immunotherapeutic approach against vaginal disease. We are also interested in identifying the immunomodulatory role of estrogen in mediating susceptibility to disease using emerging transcriptomic technologies (e.g. RNA-seq, nanoString).

 Polymicrobial intra-abdominal infection:

Microorganisms rarely exist as single species communities but instead exist within multi-species consortia where mutually beneficial, parasitic, and antagonistic interactions may develop. However, relatively little is known about the functional consequences of these interactions as they relate to health and disease.

We aim to determine the complex inter-microbial signaling events that mediate infectious synergism observed during intra-abdominal infection with the ubiquitous bacterial pathogen Staphylococcus aureus and the fungus C. albicans. Current studies are focused on identifying activation of the S. aureus agr-quorum sensing system and downstream toxins as key pathways contributing to lethal infection. The polymicrobial intra-abdominal infection serves as an excellent model system for determining microbe-microbe induced virulence gene regulation in vivo. Identification of virulence determinants may serve as rationale for selection of vaccine candidates to reduce lethality clinically associated with fungal-bacterial mixed intra-abdominal infection.

Research Keywords

vaginitis, inflammasome, estrogen, immunity, innate, immunology, fungal, pathogenesis, Candida albicans, Staphylococcus aureus, biofilm, toxin, intra-abdominal

Research Interest/Specialty

Fungal pathogenesis

Mucosal immunology

Microbiology

Publications

  1. Bruno, VM, Shetty, AC, Yano, J, Fidel, PL, Noverr, MC, Peters, BM. Transcriptomic analysis of vulvovaginal candidiasis identifies a role for the NLRP3 inflammasome. MBio, 6 (2), 2015.
  2. Schlecht, LM, Peters, BM, Krom, BP, Freiberg, JA, Hänsch, GM, Filler, SG, Jabra-Rizk, MA, Shirtliff, ME. Systemic Staphylococcus aureus infection mediated by Candida albicans hyphal invasion of mucosal tissue. Microbiology, 161 (Pt 1), 168-81, 2015.
  3. Peters, BM, Yano, J, Noverr, MC, Fidel, PL. Candida vaginitis: when opportunism knocks, the host responds. PLoS Pathog, 10 (4), e1003965, 2014.
  4. Yano, J, Palmer, GE, Eberle, KE, Peters, BM, Vogl, T, McKenzie, AN, Fidel, PL. Vaginal epithelial cell-derived S100 alarmins induced by Candida albicans via pattern recognition receptor interactions are sufficient but not necessary for the acute neutrophil response during experimental vaginal candidiasis. Infect Immun, 82 (2), 783-92, 2014.
  5. Peters, BM, Palmer, GE, Nash, AK, Lilly, EA, Fidel, PL, Noverr, MC. Fungal morphogenetic pathways are required for the hallmark inflammatory response during Candida albicans vaginitis. Infect Immun, 82 (2), 532-43, 2014.
  6. Peters, BM, Noverr, MC. Candida albicans-Staphylococcus aureus polymicrobial peritonitis modulates host innate immunity. Infect Immun, 81 (6), 2178-89, 2013.
  7. Peters, BM, Ward, RM, Rane, HS, Lee, SA, Noverr, MC. Efficacy of ethanol against Candida albicans and Staphylococcus aureus polymicrobial biofilms. Antimicrob Agents Chemother, 57 (1), 74-82, 2013.
  8. Peters, BM, Ovchinnikova, ES, Krom, BP, Schlecht, LM, Zhou, H, Hoyer, LL, Busscher, HJ, van der Mei, HC, Jabra-Rizk, MA, Shirtliff, ME. Staphylococcus aureus adherence to Candida albicans hyphae is mediated by the hyphal adhesin Als3p. Microbiology, 158 (Pt 12), 2975-86, 2012.
  9. Peters, BM, Jabra-Rizk, MA, O'May, GA, Costerton, JW, Shirtliff, ME. Polymicrobial interactions: impact on pathogenesis and human disease. Clin Microbiol Rev, 25 (1), 193-213, 2012.
  10. Xu, Z, Li, L, Shirtliff, ME, Peters, BM, Li, B, Peng, Y, Alam, MJ, Yamasaki, S, Shi, L. Resistance class 1 integron in clinical methicillin-resistant Staphylococcus aureus strains in southern China, 2001-2006. Clin Microbiol Infect, 17 (5), 714-8, 2011.
  11. Peters, BM, Jabra-Rizk, MA, Scheper, MA, Leid, JG, Costerton, JW, Shirtliff, ME. Microbial interactions and differential protein expression in Staphylococcus aureus -Candida albicans dual-species biofilms. FEMS Immunol Med Microbiol, 59 (3), 493-503, 2010.