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Debora Foster
Professor
Graduate Program Director,
Molecular Science Program

B.Sc. (University of Toronto)
M.Sc. (University of Toronto)
Ph.D. (University of Toronto)
 

 


Contact Info:

Tel: (416) 979-5000 ext. 4613
Fax: (416) 979-5044
Email: dfoster@ryerson.ca

Research Laboratory: KHE 320
Tel: 416-979-5000 ext 6525


Research Appointments and Professional Affiliations:

Cross-appointments:
Graduate Faculty, Faculty of Dentistry, University of Toronto
(http://www.utoronto.ca/dentistry/facultyresearch/units/microbiology.html#faculty)

Research Consultant, Research Institute, Hospital for Sick Children
(http://www.sickkids.ca/research)

Professional Memberships:

American Society for Microbiology (http://www.asm.org)

Canadian Association of Gastroenterologists (http://www.cag-acg.org)

Courses Taught:

Graduate Courses:
Molecular Recognition (MS8105)

This course is offered to graduate students in the Molecular Science Graduate Program. For more information, please see:

http://www.ryerson.ca/graduate/programs/molecular_science/molecularscience.courses.html

Undergraduate Courses:
Immunology (BLG 856)
Intermediary Metabolism (CHY 361)

These courses are offered to undergraduates in the third or fourth year of Bachelor Science programs in chemistry and biology.

For more information, please see http://www.ryerson.ca/calendar.

 

Research Interests:

My research focuses on host-pathogen interactions with particular emphasis on the molecular

basis of pathogenesis and the impact of environmental stress on pathogen virulence. Two

gastrointestinal pathogens, enterohemorrhagic and enteropathogenic Escherichia coli are the

subject of our current research. Enterohemorrhagic Escherichia coli causes acute

gastroenteritis, bloody diarrhea, and, in some cases, can progress to life-threatening sequelae

including hemolytic uremic syndrome. Enteropathogenic Escherichia coli causes severe

infantile diarrhea and is responsible for the death up to one million infants per year,

particularly in developing countries.



Impact of Environmental Stress on Virulence:

These pathogens are exposed a variety of stresses during ingestion as well as acid stress during food processing and we are examining how these stresses affect virulence including host adhesion, motility, toxin production and antibiotic resistance. We are currently using DNA microarray and real time PCR technology to investigate changes in virulence gene expression after numerous environmental stresses. The results of this research can have profound implications for management of these infections as well as for food handling and processing practices, since contaminated food is often the vehicle for infection. Our research on bile salt stress was profiled in an interview on the radio program,MicrobeWorld (http://www.flpradio.com/microbeworld/2008-OCT-16-31.htm). We are also examining the role of DNA repair mechanisms in acid-stressed survival of these pathogens and how inhibition of DNA repair using antimicrobial peptides can enhance acid-induced killing. This research may provide new food processing options as antimicrobial prevention strategies.

 


Apoptotic and necrotic cells can be detected by fluorescent microscopy of cells stained with eithidium bromide and acridine orange

 

Molecular Basis of Pathogenesis:

Since bacterial attachment to host cells represents the first opportunity to disrupt the bacteria-host interaction, we are particularly interested in identifying and understanding bacterial adhesin-host receptor interactions. We are currently examining the role of several afimbrial and fimbrial bacterial adhesins in mediating host adherence before and after exposure to various environment stresses. Our earlier research explored the role of host membrane phospholipids and glycolipids as membrane receptors and how these lipids are involved in host cell signaling events triggered by bacterial infection. These signaling events play critical roles in the apoptotic/mitotic balance within the cell.

 

Research Grants:

NSERC Discovery Grants (2002-2006, 2006-ongoing)
Crohn's and Colitis Research Grant (1998-2001)
NSERC Equipment Grants (multiple years)
RU Summer and winter Research Assistant Grants (multiple years)

Selected Publications and Presentations:

J.V. Kus, A. Gebremedhin, V. Dang, S.L.Tran, A. Serbanescu, D. Barnett Foster, 2011. Bile salts induce resistance to polymyxin in Enterohemorrhagic Escherichia coli O157:H7. (http://www.ncbi.nlm.nih.gov/pubmed/21725004) J. Bacteriology 193(17):4509.

M. Lino, J.V. Kus, S.L Tran, Z. Naqvi, B. Binnington, S.D. Goodman, A.M. Segall, D. Barnett Foster, 2011. A novel antimicrobial peptide significantly enhances acid-induced killing Shiga-toxin producing Escherichia coli O157 and non-O157 serotypes. Microbiology 157:1768.

B. House, J. Kus, N. Prayitno, R. Mair, L. Que, F. Chingcuanco, V. Gannon, D. Cvitkovitch, D. Barnett Foster. 2009. Acid Stress Induced Changes in Enterohemorrhagic Escherichia coli O157:H7 Virulence. Microbiology, 155:2907-2918.

J. Kus, M. Lino, Z. Naqvi, S. Goodman, A. Segall, D. Barnett Foster. February 2010. A novel antimicrobial peptide significantly reduces survival of acid-stressed pathogenic Escherichia coli Canadian Journal of Gastroenterology, CDDW 2010 Vol1: Supp SA.

Brand, S., Solanki, B., Foster, D. B.., Czarnota, G., Kolios, M 2009. Monitoring of apoptosis in epithelial cells using high frequency ultrasound spectroscopy. Ultrasound in Medicine and Biology, 35(3): 482-493.

J.V. Kus, A. Serbanescu, N. Prayitano, M. Zoubarev, V. Dang, V. Gannon, D. Barnett Foster Bile Salts induce changes in Esccherichia coli O157:H7 virulence. 7th International Symposium on Shiga Toxin (Verocytotoxin) Producing Escherichia coli Infections (VTEC2009) Buenos Aires, Argentina, May 10-13, 2009

F. Chingcuanco, C, Levesque and D. Barnett Foster. Role of a Novel Fimbrial Adhesin in Acid-induced Host Adhesion of Escherichia coli O157:H7 American Society for Microbiology 109th General Meeting, Philadelphia. May 17-21, 2009.

N.R. Prayitno, M.A. Syed and D. Barnett Foster. Impact of Bile Salt Stress on Virulence Properties of Escherichia coli O157:H7. American Society for Microbiology General Meeting, Toronto, Ontario. May 20-25, 2007.

B. House, R. Mair, D. Cvitkovitch, V. Gannon, D. Barnett Foster. Stress-Induced Changes in Enterohemorrhagic Escherichia coli O157 Virulence. Sixth International Symposium on Shiga Toxin (Verocytotoxin) Producing E. coli Infections (VTEC 2006) Melbourne, Australia, Oct 29-Nov 4, 2006.

B. J. House, R. W. Mair, D. G. Cvitkovitch, V. Gannon, D. Barnett Foster. Microarray Analysis of Acid-induced Changes in Enterohemorrhagic Escherichia coli O157 Virulence. American Society for Microbiology General Meeting, Orlando, Florida. May 20-25, 2006.

DeJesus, M., Urban, A., Marasigan, M. and D.E. Barnett Foster. 2005. Acid and Bile Salt Shock of Enteropathogenic Escherichia coli Enhances adhesion to epithelial cells and alters glycolipid receptor binding specificity. Journal of Infectious Diseases 192(8): 1430-1440.

Y. Wu, B. Lau, S. Smith, K. Troyan, and D. E. Barnett Foster 2004. Enteropathogenic Escherichia coli infection triggers host phospholipid metabolism perturbations. Infection and Immunity 72(12): 6764-6772.