Kim Lewis

Kim LewisUniversity Distinguished Professor
Director, Antimicrobial Discovery Center

Molecular Microbiology

Department of Biology
Northeastern University
306C Mugar Life Sciences
360 Huntington Avenue
Boston, MA 02115 USA
617.373.8238
k.lewis@neu.edu

Lab Website: http://www.northeastern.edu/adc/

Academic Education

  • Ph.D., Biochemistry, Moscow University, Moscow, USSR
  • B.Sc., Biology, Moscow University, Moscow, USSR

Appointments

  • Professor, Northeastern University, 7/1/01 – present

Research Interests

The focus of my research is on antimicrobial drug tolerance and drug discovery. Microorganisms produce persister cells, which are dormant variants that are highly tolerant to killing by all known antibiotics. Persisters are largely responsible for relapsing chronic infections caused by biofilms. Using transcriptome analysis, cell sorting and whole genome sequencing we are identifying genes responsible for persister formation. Both drug tolerance and conventional drug resistance require development of new antibiotics, and our discovery efforts include screening compounds from previously “uncultured” species of microorganisms, and high-throughput screening for compounds with novel mode of action.

Teaching Activities

I teach General Microbiology and Microbial Biotechnology.

Publications

  • Google Scholar
  • Conlon, B.P.,  Nakayasu, E.S.,  Fleck, L.E., LaFleur, M.D., Isabella, V.M., Coleman, K., Leonard, S.N., Smith, R.D., Adkins, J.N. and Lewis, K. (2013) Protease activation kills persisters and eradicates a chronic biofilm infection. Nature 503: 365-370.
  • K Lewis (2013) Platforms for antibiotic drug discovery. Nature Reviews Drug Discovery. 12, 371–387.[PDF]
  • I Keren, Y Wu, J Inocencio, LR Mulcahy, K Lewis (2013) Killing by bactericidal antibiotics does not depend on reactive oxygen species. Science. 339 (6124), 1213-1216. [PDF]
  • Sonja Hansen, Marin Vulic, Jungki Min, Tien-Jui Yen, Maria A. Schumacher, Richard G. Brennan, Kim Lewis (2012) Regulation of the Escherichia coli hipBA toxin-antitoxin system by proteolysis. PLoS ONE. 7(6):e39185. [PDF]
  • Kim Lewis (2012) Antibiotics: Recover the lost art of drug discovery. Nature. 485:439-440. [PDF]
  • Keren I, Minami S, Rubin E, and Kim Lewis (2011) Characterization and transcriptome analysis of Mycobacterium tuberculosis. mBio. 2(3):e00100-11. [PDF]
  • Lawrence R. Mulcahy, Jane L. Burns, Stephen Lory, and Kim Lewis (2010) Emergence of Pseudomonas aeruginosa strains producing high levels of persister cells in patients with cystic fibrosis. J. Bacteriol. 192(23):6191-99. [PDF]
    • Nature Medicine. (2011) Persistence may pay off for antibiotics innovators. 17:652. (News) Michelle Pflumm.
    • Microbe Magazine. (2011) Persister cells fingered in chronic CF. (Feature).
  • Kim Lewis (2010) Persister Cells. Annu. Rev. Microbiol. 64:357-72. [PDF]
  • Anthony D’Onofrio, Jason M. Crawford, Eric J. Stewart, Kathrin Witt, Ekaterina Gavrish, Slava Epstein, Jon Clardy, Kim Lewis (2010) Siderophores from neighboring organisms promote the growth of uncultured bacteria. Chemistry & Biology. 17(3):256-264. [PDF]
    • Microbe Magazine. (2010) Siderophores shed light on the “Great Plate Count Anomaly”. (Feature & Podcast) Carol Potera. [PDF]
    • ASM Blog. (2010) Small Things Considered: The uncultured bacteria. Kim Lewis. [PDF]
  • Dörr T, Vulic M, Lewis K (2010) Ciprofloxacin causes persister formation by inducing the TisB toxin in Escherichia coli. PloS Biology 8(2):e1000317. [PDF]
  • Michael D. LaFleur, Qingguo Qi, and Kim Lewis. (2010) Patients with long-term oral carriage harbor high-persister mutants of C. albicans. Antimicrob. Agents Chemother. 54(1):39-44. [PDF]
  • Dörr T, Lewis K, Vulic M (2009) SOS response induces persistence to fluoroquinolones in Escherichia coli. PloS Genetics. 5(12):e1000760. [PDF]
  • Schumacher MA, Piro KM, Xu W, Hansen S, Lewis K, Brennan RG. (2009) Molecular mechanisms of HipA-mediated multidrug tolerance and its neutralization by HipB. Science. 323(5912):396-401. [PDF]