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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://www.dartmouth.edu/~hoganlab
http://www.dartmouth.edu/~molpath/
http://www.dartmouth.edu/~mcb/

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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).


Selected Publications

 

Conserved C-Terminal Tail Is Responsible for Membrane Localization and Function of Pseudomonas aeruginosa Hemerythrin.
Stuut Balsam S, Zhong F, Pence N, Levintov L, Andhare D, Hammond JH, Ragusa MJ, Vashisth H, Hogan DA, Pletneva EV
Biochemistry. 2024 Jul 1; doi: 10.1021/acs.biochem.4c00174. Epub 2024 Jul 1.
PMID: 38951132

Widespread fungal-bacterial competition for magnesium lowers bacterial susceptibility to polymyxin antibiotics.
Hsieh YP, Sun W, Young JM, Cheung R, Hogan DA, Dandekar AA, Malik HS
PLoS Biol. 2024 Jun;22(6):e3002694. doi: 10.1371/journal.pbio.3002694. Epub 2024 Jun 20.
PMID: 38900845

Loss of LasR function leads to decreased repression of Pseudomonas aeruginosa PhoB activity at physiological phosphate concentrations.
Conaway A, Todorovic I, Mould DL, Hogan DA
bioRxiv. 2024 May 1; pii: 2024.03.27.586856. doi: 10.1101/2024.03.27.586856. Epub 2024 May 1.
PMID: 38585852

P. aeruginosa tRNA-fMet halves secreted in outer membrane vesicles suppress lung inflammation in cystic fibrosis.
Li Z, Barnaby R, Nymon A, Roche C, Koeppen K, Ashare A, Hogan DA, Gerber SA, Taatjes DJ, Hampton TH, Stanton BA
Am J Physiol Lung Cell Mol Physiol. 2024 May 1;326(5):L574-L588. doi: 10.1152/ajplung.00018.2024. Epub 2024 Mar 5.
PMID: 38440830

How P. aeruginosa cells with diverse stator composition collectively swarm.
de Anda J, Kuchma SL, Webster SS, Boromand A, Lewis KA, Lee CK, Contreras M, Medeiros Pereira VF, Schmidt W, Hogan DA, O'Hern CS, O'Toole GA, Wong GCL
mBio. 2024 Apr 10;15(4):e0332223. doi: 10.1128/mbio.03322-23. Epub 2024 Mar 1.
PMID: 38426789

Pseudomonas aeruginosa transcriptome analysis of metal restriction in ex vivo cystic fibrosis sputum.
Neff SL, Doing G, Reiter T, Hampton TH, Greene CS, Hogan DA
Microbiol Spectr. 2024 Apr 2;12(4):e0315723. doi: 10.1128/spectrum.03157-23. Epub 2024 Feb 22.
PMID: 38385740

Citrate cross-feeding by Pseudomonas aeruginosa supports lasR mutant fitness.
Mould DL, Finger CE, Conaway A, Botelho N, Stuut SE, Hogan DA
mBio. 2024 Feb 14;15(2):e0127823. doi: 10.1128/mbio.01278-23. Epub 2024 Jan 23.
PMID: 38259061

Bacterial Outer Membrane Vesicles and Immune Modulation of the Host.
Charpentier LA, Dolben EF, Hendricks MR, Hogan DA, Bomberger JM, Stanton BA
Membranes (Basel). 2023 Aug 24;13(9) doi: 10.3390/membranes13090752. Epub 2023 Aug 24.
PMID: 37755174

Analysis of Pseudomonas aeruginosa transcription in an ex vivo cystic fibrosis sputum model identifies metal restriction as a gene expression stimulus.
Neff SL, Doing G, Reiter T, Hampton TH, Greene CS, Hogan DA
bioRxiv. 2023 Aug 21; pii: 2023.08.21.554169. doi: 10.1101/2023.08.21.554169. Epub 2023 Aug 21.
PMID: 37662412

Comparative effects of CFTR modulators on phagocytic, metabolic and inflammatory profiles of CF and nonCF macrophages.
Aridgides DS, Mellinger DL, Gwilt LL, Hampton TH, Mould DL, Hogan DA, Ashare A
Sci Rep. 2023 Jul 25;13(1):11995. doi: 10.1038/s41598-023-38300-9. Epub 2023 Jul 25.
PMID: 37491532

View more publications on PubMed