James E. Bina, PhD

  • Professor, Department of Microbiology and Molecular Genetics
  • Member, Graduate Program in Microbiology and Immunology (PMI)

Education & Training

  • Post Doctoral Training, Department of Microbiology and Immunobiology, Harvard Medical School
  • PhD, University of British Columbia
  • MSc, BSc, University of Wisconsin-Madison

Research Interest Summary

Bacteriology, Antibiotic Resistance, Pathogenesis, Host Pathogenesis

Research Interests

The Bina lab studies antimicrobial resistance and bacterial pathogenesis in the gram-negative pathogens Vibrio cholerae and Klebsiella pneumoniae. The log-term goal of our studies are to define the mechanisms that bacteria use to cause human disease and to develop novel therapeutic approaches to circumvent antibiotic resistance.

The major focus of the lab is on V. cholerae which is an aquatic organism that causes the epidemic diarrheal disease cholera. Cholera affects ~5 million people each year, primarily in developing regions of the world. A major focus of our lab is to elucidate the function of RND-family multidrug efflux systems in bacterial biology. RND systems are ubiquitous transporters in gram negative bacteria that provide cross-resistance to multiple antimicrobials. This makes them crucial for the development of antibiotic resistance. However, the native functions of the RND systems are unknown. We have shown that the RND systems are required for V. cholerae pathogenesis. Mutation of the RND systems results in cells that are no longer able to express virulence genes or persist in the host gastrointestinal tract. These findings validated the RND systems as novel targets for the development of antivirulence and antimicrobial therapeutics. Ongoing work is focused on characterizing the molecular mechanisms that link efflux to V. cholerae biology and identifying novel inhibitors of the RND efflux systems.

Recently we expanded our studies to Klebsiella pneumoniae. K. pneumoniae is an understudied gram-negative pathogen that causes a multitude of healthcare-associated infections including pneumonia, bloodstream infections, urinary tract infections, wound or surgical site infections, and meningitis. K. pneumoniae has rapidly evolved resistance to all clinically relevant antibiotics which has landed it on the priority 1 list of pathogens published by the World Health Organization. We are working to define and characterize the intrinsic mechanisms that allow K. pneumoniae to resist antibiotics and persist in humans during infection.


Bina XR, Howard MF, Taylor-Mulneix DL, Ante VM, Kunkle DE, Bina JE. The Vibrio cholerae RND efflux systems impact virulence factor production and adaptive responses via periplasmic sensor proteins. PLoS Pathog. 2018;14(1):e1006804. Epub 2018/01/06. doi: 10.1371/journal.ppat.1006804. PubMed PMID: 29304169; PMCID: PMC5773229.

Bina TF, Kunkle DE, Bina XR, Mullett SJ, Wendell SG, Bina JE. Bile Salts Promote ToxR Regulon Activation during Growth under Virulence-Inducing Conditions. Infect Immun. 2021;89(12):e0044121. Epub 2021/09/21. doi: 10.1128/IAI.00441-21. PubMed PMID: 34543121; PMCID: PMC8594600.

Weng Y, Bina TF, Bina XR, Bina JE. ToxR Mediates the Antivirulence Activity of Phenyl-Arginine-beta-Naphthylamide To Attenuate Vibrio cholerae Virulence. Infect Immun. 2021;89(7):e0014721. Epub 2021/05/05. doi: 10.1128/IAI.00147-21. PubMed PMID: 33941578; PMCID: PMC8208513.

Kunkle DE, Bina XR, Bina JE. The Vibrio cholerae VexGH RND Efflux System Maintains Cellular Homeostasis by Effluxing Vibriobactin. mBio. 2017;8(3). Epub 2017/05/18. doi: 10.1128/mBio.00126-17. PubMed PMID: 28512090; PMCID: PMC5433094.

Kunkle DE, Bina TF, Bina XR, Bina JE. Vibrio cholerae OmpR Represses the ToxR Regulon in Response to Membrane Intercalating Agents That Are Prevalent in the Human Gastrointestinal Tract. Infect Immun. 2020;88(3). Epub 2019/12/25. doi: 10.1128/IAI.00912-19. PubMed PMID: 31871096; PMCID: PMC7035920.