Deborah A Hogan, PhD
Professor of Microbiology and Immunology
Microbiology and Immunology
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.
Dewey Field Rd. HB7550
Hanover NH 03755
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).
<i>Pseudomonas aeruginosa</i> Alginate Overproduction Promotes Coexistence with <i>Staphylococcus aureus</i> in a Model of Cystic Fibrosis Respiratory Infection.
Global Role of Cyclic AMP Signaling in pH-Dependent Responses in <i>Candida albicans</i>.
ADAGE-Based Integration of Publicly Available <i>Pseudomonas aeruginosa</i> Gene Expression Data with Denoising Autoencoders Illuminates Microbe-Host Interactions.
Signaling through Lrg1, Rho1 and Pkc1 Governs Candida albicans Morphogenesis in Response to Diverse Cues.
Environmentally Endemic Pseudomonas aeruginosa Strains with Mutations in lasR Are Associated with Increased Disease Severity in Corneal Ulcers.
Use of a Multiplex Transcript Method for Analysis of Pseudomonas aeruginosa Gene Expression Profiles in the Cystic Fibrosis Lung.
A Novel Mechanism of Host-Pathogen Interaction through sRNA in Bacterial Outer Membrane Vesicles.
The Pseudomonas aeruginosa efflux pump MexGHI-OpmD transports a natural phenazine that controls gene expression and biofilm development.
Analysis of Lung Microbiota in Bronchoalveolar Lavage, Protected Brush and Sputum Samples from Subjects with Mild-To-Moderate Cystic Fibrosis Lung Disease.
Mitochondrial Activity and Cyr1 Are Key Regulators of Ras1 Activation of C. albicans Virulence Pathways.