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Deborah A Hogan, Ph.D.

Associate 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.

National Center for Disaster Mental Health Research

NIH Biosketch:


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:


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:


Torres IM, Patankar YR, Shabaneh TB, Dolben E, Hogan DA, Leib DA, Berwin BL
Acidosis Potentiates the Host Pro-Inflammatory IL-1β Response to Pseudomonas aeruginosa Infection.
Infect Immun 2014 Aug 25;
PMID: 25156732

Jackson AA, Daniels EF, Hammond JH, Willger SD, Hogan DA
The global regulator Anr represses PlcH phospholipase activity in Pseudomonas aeruginosa when oxygen is limiting.
Microbiology 2014 Jul 29;
PMID: 25073853

Hogan D, Wheeler RT
The complex roles of NADPH oxidases in fungal infection.
Cell Microbiol 2014 Aug; 16(8):1156-67
PMID: 24905433

Price KE, Hampton TH, Gifford AH, Dolben EL, Hogan DA, Morrison HG, Sogin ML, O'Toole GA
Unique microbial communities persist in individual cystic fibrosis patients throughout a clinical exacerbation.
Microbiome 2013 Nov 1; 1(1):27
PMID: 24451123

Piispanen AE, Grahl N, Hollomon JM, Hogan DA
Regulated proteolysis of Candida albicans Ras1 is involved in morphogenesis and quorum sensing regulation.
Mol Microbiol 2013 Jul; 89(1):166-78
PMID: 23692372

Hogan DA, Hammond JH
Bacterial type 6 secreted phospholipases play family feud.
Cell Host Microbe 2013 May 15; 13(5):507-8
PMID: 23684302

Morales DK, Grahl N, Okegbe C, Dietrich LE, Jacobs NJ, Hogan DA
Control of Candida albicans metabolism and biofilm formation by Pseudomonas aeruginosa phenazines.
MBio 2013 Jan 29; 4(1):e00526-12
PMID: 23362320

Lindsay AK, Deveau A, Piispanen AE, Hogan DA
Farnesol and cyclic AMP signaling effects on the hypha-to-yeast transition in Candida albicans.
Eukaryot Cell 2012 Oct; 11(10):1219-25
PMID: 22886999

Ballok AE, Bahl CD, Dolben EL, Lindsay AK, St Laurent JD, Hogan DA, Madden DR, O'Toole GA
Epoxide-mediated CifR repression of cif gene expression utilizes two binding sites in Pseudomonas aeruginosa.
J Bacteriol 2012 Oct; 194(19):5315-24
PMID: 22843844

Malek AA, Wargo MJ, Hogan DA
Absence of membrane phosphatidylcholine does not affect virulence and stress tolerance phenotypes in the opportunistic pathogen Pseudomonas aeruginosa.
PLoS One 2012; 7(2):e30829
PMID: 22363496