Deborah A Hogan, PhD
Title(s):
Professor of Microbiology and Immunology
Department(s):
Microbiology and Immunology
Education:
Michigan State University, Ph.D., 1999
Harvard University, A.B., 1993
Dr. Hogan received her A.B. degree in Biology from Harvard University in
1993, and her Ph.D. in Microbiology from the Michigan State University in
1999. After postdoctoral work at Harvard Medical School, Dr. Hogan joined
the faculty of the Department of Microbiology and Immunology at Dartmouth Medical School in 2004.
Websites:
http:
http:
http:
Contact Information:
Vail Building#208
Dewey Field Rd. HB7550
Hanover NH 03755
Phone: 603-650-1252
Fax: 603-650-1318
Email: Deborah.A.Hogan@Dartmouth.edu
Professional Interests:
MICROBE-MICROBE INTERACTIONS
The interactions between different microbial species govern the activity of microbial communities, whether they be in association with a host or free-living in the environment. Microbial communities have very significant effects on human health. For example, synergistic relationships between the organisms within the human microflora confer protection against pathogens and enable the degradation of complex substrates. At the same time, many illnesses, such as respiratory and genital infections, gastroenteritis, and periodontal diseases, often involve multiple microorganisms. In the Hogan Lab, we are interested in understanding the molecular basis for such interactions by describing the mechanisms by which one microbe affects the physiology, survival, and virulence properties of another microbial species.
Our lab primarily focuses on the interactions between the Gram-negative bacterium Pseudomonas aeruginosa and the dimorphic fungus, Candida albicans. These two organisms co-exist within diverse opportunistic human infections, and clinical observations suggest that P. aeruginosa inhibits C. albicans growth. In our in vitro system, we observe that the bacteria physically attach to the fungal filaments, form biofilms on their surfaces, and kill the fungal cells. Many of the bacterial factors used to kill the fungus also participate in P. aeruginosa virulence towards humans. The fungus responds to the presence of the P. aeruginosa by reverting to a resistant yeast form. We are using genetic screening methods, analysis of defined mutants, biochemical approaches and genomic profiling techniques to better understand the bacterial and fungal factors that are involved in this relationship. By studying the interactions between microbial species, we are learning about important elements relating to the physiology and pathogenesis of the individual microbes. in addition to gaining insight in to how microbial communities function.
For more information, please visit the Hogan Lab Home Page (www.dartmouth.edu/~hoganlab).
Selected Publications: |
|
Editorial overview of Pearls Microbiome Series: E pluribus unum. Let-7b-5p in vesicles secreted by human airway cells reduces biofilm formation and increases antibiotic sensitivity of P. aeruginosa. Both Pseudomonas aeruginosa and Candida albicans Accumulate Greater Biomass in Dual-Species Biofilms under Flow. Intraspecies heterogeneity in microbial interactions. Calprotectin-Mediated Zinc Chelation Inhibits Pseudomonas aeruginosa Protease Activity in Cystic Fibrosis Sputum. Balancing Positive and Negative Selection: In Vivo Evolution of Candida lusitaniae MRR1. Debaryomyces is enriched in Crohn's disease intestinal tissue and impairs healing in mice. Mrr1 regulation of methylglyoxal catabolism and methylglyoxal-induced fluconazole resistance in Candida lusitaniae. Correcting for experiment-specific variability in expression compendia can remove underlying signals. Intraspecies Signaling between Common Variants of Pseudomonas aeruginosa Increases Production of Quorum-Sensing-Controlled Virulence Factors. |
|