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Biofilm-associated Infection



DESCRIPTION OF LAB RESEARCH WORK

Our laboratory is working to understand the bacterial factors that contribute to colonization, biofilm formation, and infection by Enterococus faecalis and related pathogens. We focus on infection in wounds, the urinary tract, and the gastrointestinal tract.

LAB MEMBERS
LEAD PI ​
Kimberly Kline
Associate Chair (Students), School of Biological Sciences
Assistant Dean (Special Projects), College of Science
Associate Professor, School of Biological Sciences

Email: kkline@ntu.edu.sg
Phone: (65) 6592 7943
Office: SBS-B1N-27
Lab webpage
Ch'ng Jun Hong
Affiliated Principal Investigator

Email: micchn@nus.edu.sg
Dr Anuradha Vajjala
Research Fellow

Email: anuradhav@ntu.edu.sg​
Artur Matysik
Research Fellow

Email: arturmatysik@ntu.edu.sg​
Irina Afonina
Postdoc Associate

Email: irina@smart.mit.edu​
Choo Pei Yi
Research Assistant

Email: pychoo@ntu.edu.sg​
Ho Foo Kiong
Research Assistant

Email: hofk@ntu.edu.sg​
Bala Davient
PhD Student

Email: bala0044@e.ntu.edu.sg​
Brenda Tien Yin Qi
PhD Student

Email:btien002@e.ntu.edu.sg
Casandra Tan
PhD Student

Email: TANA0032@e.ntu.edu.sg​
Chen Qingyan
PhD Student

Email: CHEN1014@e.ntu.edu.sg
Kao Hsien Neng, Patrick
PhD Student

Email: S170024@e.ntu.edu.sg
Nair Zeus Jaren
PhD Student

Email: nairzeus001@e.ntu.edu.sg​
Wong Jun Jie
PhD Student

Email: jjwong@ntu.edu.sg​


CURRENT PROJECTS
Project Title: Pathogenesis of Biofilm-Associated Infections
The Gram-positive Enterococci are commensal inhabitants of the gastrointestinal tract, as well as opportunistic pathogens associated with endocarditis, urinary tract infections, wound infection, and dysbiosis in the gut. Many Enterococcal infections are difficult to treat due to their multi-drug resistance, association with bacterial biofilms, and polymicrobial nature. The goal of our research is to understand the molecular mechanisms by which Enterococcus faecalis (and closely related pathogens such as Group A Streptococcus) interacts with other bacterial species and the host in the context of these polymicrobial, biofilm-associated infections.

Project Title: The Cell Biology of Enterococcus Faecalis Infection
Enterococcus faecalis is one of most frequently isolated bacterial species in wounds yet little is known about its pathogenic mechanisms in this setting. We have characterized a mouse excisional wound model to study the infection dynamics of E. faecalis and shown that infected wounds are associated with acute bacterial replication, long term persistence within the wounds, and delayed wound healing. Enterococci are also immunosuppressive and have niche-modulatory capacities that promote their virulence, as well as that of co-infecting organisms. This project seeks to identify the mechanisms by which E. faecalis suppresses the host immune response to promote intracellular survival and persistence.

Project Title: Mechanism of Focal Virulence Factor Assembly in Enterococcus Faecalis
Bacterial factors responsible for interaction with the environment or host, such as pili, are often found on the cell surface. In Gram positive bacteria, sortase enzymes are responsible for both pilus polymerization as well as the attachment of polymerized pili, as well as some other secreted proteins, to the bacterial cell wall. Sortase enzymes colocalize with the general secretion machinery in E.
faecalis at discrete septum-associated foci, resulting in spatially restricted sites of pilus virulence factor assembly. In this project, we are exploring the molecular mechanisms that dictate focal localization of virulence factor assembly sites, using the pilus assembly platform as a model system.

PUBLICATIONS
Full list of publications can be found here
  • Ch’ng JH, Chong KKL, Lam LN, Wong JJ, Kline KA. (2018) Biofilm-associated infection by Enterococci. Nature Reviews Microbiology. Jan;17(2):82-94. doi: 10.1038/s41579-018-0107-z.
  • Vajjala A, Biswas D, Tay WH, Hanski E, Kline KA. (2018) Streptolysin-induced endoplasmic reticulum stress promotes group A streptococcal in vivo biofilm formation and necrotizing fasciitis. Cellular Microbiology. Jan;21(1):e12956.
  • Afonina I, Lim XN, Tan R, Kline KA. (2018) Planktonic interference and biofilm alliance between aggregation substance and endocarditis and biofilm associated pili in Enterococcus faecalis. Journal of Bacteriology. Nov 26;200(24).
  • Keogh D*, Lam LN*, Doyle L, Matysik A, Pavagadhi S, Umashankar S, Dale J, Dunny G, Swarup S, Williams RBH, Marsili E, Kline KA. (2018) Extracellular electron transfer in Enterococcus faecalis biofilm metabolism. *Authors contributed equally. mBio 10 April vol. 9 no. 2 e00626-17.
  • Chong K, Tay WH, Janela B, Yong AMH, Liew TH, Madden L, Keogh D, Barkham T, Ginhoux F, Becker D, Kline KA. (2017) Enterococcus faecalis modulates immune activation and slows healing during wound infection. Journal of Infectious Disease. 216(12):1644-1654.
  • Tien B*, Goh S*, Chong K*, Tagore S*, Holec S, Ingersoll MA, Ginhoux F, Williams RB, Kline KA. (2017) Enterococcus faecalis modulates the host response and promotes polymicrobial catheter-associated urinary tract infection. *Authors contributed equally. Infection & Immunity. 85:12 14.
  • Keogh D, Tay WH, Ho YY, Dale J, Chen S, Umashankar S, Williams RBH, Chen SL, Dunny G, Kline KA. (2016) Enterococcal metabolite cues facilitate interspecies niche modulation and polymicrobial wound infection. Cell Host & Microbe 20(4):493-503.
  • Rousseau M*, Goh S*, Holec S, Williams RBH, Ingersoll MA, Kline KA. (2016) Bladder catheterization increases susceptibility to infection that can be prevented by prophylactic antibiotic treatment. *Authors contributed equally. JCI Insight 1(15):e88178. doi:10.1172/jci.insight.88178.
  • Mitra SD*, Afonina I*, Kline KA. (2016) Right place, right time: focalization of membrane proteins in Gram-positive bacteria. *Authors contributed equally. Trends in Microbiology 24(8):611-21.
  • Kandaswamy K, Liew C, Wang CY, Meyer-Hoffert U, Huston-Warren E, Schroder J-M, Normark S, Caparon MG, Henriques-Normark B, Hultgren SJ, Kline KA. (2013) Focal targeting by human β defensin 2 disrupts localized virulence factor assembly sites in E. faecalis. PNAS 110(50):20230-5.
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