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:
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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).
Pseudomonas aeruginosa LasR-deficient mutants have increased methylglyoxal and hydrogen peroxide sensitivity due to low intracellular glutathione. Drivers of diversification in fungal pathogen populations. Conserved C-Terminal Tail Is Responsible for Membrane Localization and Function of Pseudomonas aeruginosa Hemerythrin. Widespread fungal-bacterial competition for magnesium lowers bacterial susceptibility to polymyxin antibiotics. Loss of LasR function leads to decreased repression of Pseudomonas aeruginosa PhoB activity at physiological phosphate concentrations. P. aeruginosa tRNA-fMet halves secreted in outer membrane vesicles suppress lung inflammation in cystic fibrosis. How P. aeruginosa cells with diverse stator composition collectively swarm. Pseudomonas aeruginosa transcriptome analysis of metal restriction in ex vivo cystic fibrosis sputum. Citrate cross-feeding by Pseudomonas aeruginosa supports lasR mutant fitness. Bacterial Outer Membrane Vesicles and Immune Modulation of the Host. |
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