19A Ackert Hall
(785) 532-6122
lynnh@ksu.edu

Research Focus

My research laboratory is interested in understanding the mechanisms of pathogenesis for the opportunistic bacterial pathogen, Enterococcus faecalis.  This organism now ranks as a leading cause of hospital acquired infection, causing a variety of infections ranging from urinary tract infection, bacteremia and wound infection to life threatening endocarditis.  These infections are often difficult to treat due to the presence of multiple antibiotic resistances.  One of the virulence properties of the organism of interest is the production of capsular polysaccharide.  The presence of the capsule enhances the organism’s ability to persist in the host at sites of infection. The capsule is considered to be anti-phagocytic allowing the bacterium to escape killing by neutrophils in the absence of capsule specific antibodies.  We are interested in determining the underlying genetic pathways related to the regulation and production of capsule, with the goal of identifying candidate targets for the development of new anti-infectives.  We are also examining biofilm formation by this organism to determine those factors essential to this developmental process.  Biofilms are aggregates of bacteria attached to a solid surface and are thought to be the primary mode of growth during infection.  Understanding the basis for biofilm formation will allow us to target those key factors with the goal of disrupting a process vital to the organism’s ability to cause disease.

Selected Research Publications

Hufnagel M., L.E. Hancock, S. Koch, C. Thielacker, M.S. Gilmore, and J. Huebner.  2004.  Serological and genetic diversity of capsular polysaccharides in Enterococcus faecalis.  J Clin Microbiol. 42: 2548-2557.

Hancock, L.E. and M. Perego.  2004.  The Enterococcus faecalis fsr two-component system controls biofilm development through production of gelatinase. J Bacteriol. 186:5629-5639.

Hancock, L.E. and M. Perego.  2004.  Systematic inactivation and phenotypic characterization of two-component signal transduction systems of Enterococcus faecalis V583. J Bacteriol. 186: 7951-7958.

Hancock, L.E., B.D. Shepard, and M.S. Gilmore.  2003.  Molecular analysis of the Enterococcus faecalis serotype 2 polysaccharide determinant. J. Bacteriol. 185:4393-4401.

Hancock, L.E. and M. Perego.  2002.  Two-component signal transduction in Enterococcus faecalis. J. Bacteriol. 184:5819-5825.

Coyette, J. and L.E. Hancock.  2002.  The Enterococcal Cell Wall. In: Enterococci: Pathogenesis, Molecular Biology, Antimicrobial Resistance and Infection Control; M. Gilmore, P. Courvalin, D. Clewell, G. Dunny, B. Murray, and L. Rice (eds). American Society for Microbiology, Washington D.C. p. 177-218.

Hancock, L.E. and M.S. Gilmore.  2002.  The capsular polysaccharide of Enterococcus faecalis and its relationship to other polysaccharides in the cell wall. Proc. Natl. Acad. Sci. USA  99:5474-5479.

Hancock, L.E. and M.S. Gilmore.  2000.  Pathogenicity of Enterococci. In: Gram-Positive Pathogens; V. Fischetti, R. Novick, J. Ferretti, D. Portnoy, and J. Rood (eds). American Society for Microbiology, Washington D.C. p. 251-258.

Callegan, M.C., B.D. Jett, L.E. Hancock, and M.S. Gilmore.  1999.  Role of hemolysin BL in the pathogenesis of extraintestinal Bacillus cereus infection assessed in an endophthalmitis model.  Infect. Immun. 67:3357-3366.

Coburn, P.S., L.E. Hancock, M.C. Booth, and M.S. Gilmore.  1999.  A novel means of self- protection, unrelated to toxin activation, confers immunity to the bactericidal effects of the Enterococcus faecalis cytolysin.  Infect. Immun. 67:3339-3347.