F A C U L T Y   P R O F I L E 

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PRINCE, ALICE S., M.D.
Professor of Pediatrics (Infectious Disease) in Pharmacology

Bacterial induction of cytokine signaling in epithelial cells

Office: Black Building | 4th Floor | Room 418
Telephone: 212.305.4193
Fax: 212.305.8780
Email:
asp7@columbia.edu

Prince Lab

Areas of Research

Innate immune responses to airway pathogens – Our laboratory studies the interaction of host-adapted pathogens and the airway mucosa, asking how bacteria change gene expression to maintain infection in the human lung; and how the host responds to these organisms. We use a variety of model systems; classic bacterial genetics, constructing and studying mutants to identify which gene products are important; murine models of pneumonia using a variety of mouse models as well as in vitro studies using human airway epithelial and immune cells. We are especially interested in the adaptation of clinical isolates and routinely use whole genome sequenced strains, proteomic and RNASeq analyses to query the host response to infection. Ongoing studies focus upon the carbapenem-resistant K. pneumoniae, P. aeruginosa and S. aureus.

Innate immune responses to airway pathogens
– Our laboratory studies the interaction of host-adapted pathogens and the airway mucosa, asking how bacteria change gene expression to maintain infection in the human lung; and how the host responds to these organisms. We use a variety of model systems; classic bacterial genetics, constructing and studying mutants to identify which gene products are important; murine models of pneumonia using a variety of mouse models as well as in vitro studies using human airway epithelial and immune cells. We are especially interested in the adaptation of clinical isolates and routinely use whole genome sequenced strains, proteomic and RNASeq analyses to query the host response to infection. Ongoing studies focus upon the carbapenem-resistant K. pneumoniae, P. aeruginosa and S. aureus.

MRSA pneumoniaS. aureus is a frequent cause of severe pneumonia. Using metabolomic studies, we have identified how changes in staphylococcal metabolism, specifically utilization of the TCA cycle are associated with infection. Our ongoing studies seek to identify the metabolic and cytokine signals in the airway that promote S. aureus biofilm formation and persistent pulmonary infection both in normal hosts and in cystic fibrosis patients.

Visit the Prince Lab website


Selected Publications

1. Ahn D, Wickersham M, Riquelme S, Prince A. (2018). The Effects of IFN-λ on Epithelial Barrier Function Contribute to K. pneumoniae ST258 Pneumonia. Am J Respir Cell Mol Biol. 2018 Sep 5. doi: 10.1165/rcmb.2018-0021OC. PMID: 30183325

2. Riquelme S.A, Ahn D, Prince A. (2018). Pseudomonas aeruginosa and Klebsiella pneumoniae Adaptation to Innate Immune Clearance Mechanisms in the Lung. J Innate Immun. 2018 Apr 4. doi: 10.1159/000487515. PMID: 29617698

3. Riquelme S.A., Hopkins B.D., Wolfe A.L., DiMango E., Kitur K., Parsons R., Prince A. (2017). Cystic Fibrosis Transmembrane Conductance Regulator Attaches Tumor Suppressor PTEN to the Membrane and Promotes Anti Pseudomonas aeruginosa Immunity. Immunity. 2017 Dec 19;47(6):1169-1181.e7. doi: 10.1016/j.immuni.2017.11.010. PMID: 29246444

4. Ahn, D., & Prince, A. (2017). Host-Pathogen Interface: Progress in Understanding the Pathogenesis of Infection Due to Multidrug-Resistant Bacteria in the Intensive Care Unit. J Infect Dis. 2017 Feb 15;215(suppl_1):S1-S8. doi:10.1093/infdis/jiw405.

5. Wickersham M., Wachtel S., Wong Fok Lung T., Soong G., Jacquet R., Richardson A., Parker D., & Prince A. (2017). Metabolic Stress Drives Keratinocyte Defenses against Staphylococcus aureus Infection. Cell Rep. 2017 Mar 14;18(11):2742-2751. doi: 10.1016/j.celrep.2017.02.055.