Bruce A. Stanton, PhD
Title(s)
Professor of Microbiology and Immunology
Andrew C. Vail Memorial Professorship
Additional Titles/Positions/Affiliations
Andrew C. Vail Professor
Director of the Lung Biology Center
Department(s)
Microbiology and Immunology
Education
U. Maine, BS 1974
Yale University, MS 1976
Yale University, PHD 1980
Programs
Molecular and Cellular Biology Graduate Programs
Websites
https:
Contact Information
Geisel School of Medicine
HB 7701
Hanover NH 03755
Office: 520 Remsen
Phone: 603-650-1775
Email: bas@dartmouth.edu
Professional Interests
1. Host-pathogen interactions in Cystic Fibrosis. The goal of this project is to elucidate how Pseudomonas aeruginosa infects airway epithelial cells and forms drug resistant biofilms in patients with CF, and to understand how airway epithelial cells facilitate drug resistant by Pseudomonas aeruginosa using genomic approaches, including RNA-seq and sc-RNA-seq, and proteomic approaches.
2. Host-pathogen cross talk. The goal of this project is to elucidate how extracellular vesicles secreted by the host and by pathogens regulate and modify bacterial infections in the lungs.
3. Arsenic and innate immunity. The goal of this project is to elucidate how arsenic suppresses the innate immune response to viral and bacterial infections.
Rotations and Thesis Projects
1. Host-pathogen interactions in Cystic Fibrosis.
2. Arsenic and innate immunity
3. Bioinformatics
Grant Information
Cystic Fibrosis Foundation: Research Development Program
Title: Translational Research in Cystic Fibrosis Principal Investigator: B.A. Stanton
Principal Investigator: B.A. Stanton
Project Period: 7/1/19 - 6/30/23
Cystic Fibrosis Foundation: Research Grant
P. aeruginosa siRNA-59370 inhibits the antiviral response of human bronchial epithelial cells
Principal Investigator: B.A. Stanton
Project Period: 12/01/19 - 11/30/21
National Institutes of Health (R01 HL151385-01)
Title: Let-7b in Extracellular Vesicles Secreted by Bronchial Epithelial Cells Increases the Antibiotic Sensitivity of Pseudomonas
Principal Investigator: B.A. Stanton
Project Period: 12/14/20 - 11/31/24
National Institutes of Health (R25 GM1297960)
Title: Data to Action: A secondary school-based citizen science project to address arsenic Contamination of well water.
Principal Investigator: Jane Disney
Role: PI of program in New Hampshire
Project Period: 08/01/18 - 07/31/23
National Institutes of Health (R25 HG011447)
Title: Reproducible and FAIR Bioinformatics Analysis of Omics Data
Principal Investigator: B.A. Stanton
Project Period: 12/14/20 - 11/31/24
National Institutes of Health (P30 DK117469)
Title: DartCF: Dartmouth Cystic Fibrosis Research Center
Principal Investigator: D. Madden
Role: Co-PI of Administrative Core and PI of GI Biology Core and Bioinformatics Core.
Project Period: 07/01/20 - 06/30/25
R25 HG011447 (Stanton/Hampton, Co-PIs)Reproducible and FAIR Bioinformatics Analysis of Omics Data
Co-Principal Investigator: B.A. Stanton
Project period: 12/14/20 - 11/31/25
Courses Taught
Honors 350-Molecular Mechanisms of Human Disease-INBRE-Mt Desert Island Biological Laboratory (MDIBL)
Applied Bioinformatics-MDIBL
Mentoring Information
Dr. Stanton has trained over 100 postdoctoral fellows, graduate students and undergraduates.
Biography
Biography. Dr. Stanton received his B.S. from the University of Maine 1974 and his Ph.D. from Yale University in 1980. He came to Dartmouth in 1984 as an Assistant Professor, was promoted to Associate Professor in 1988, and to Professor in 1993. Dr. Stanton has co-written and co-edited several textbooks including Renal Physiology, now in its 6th edition, and Physiology, now in its 7th edition. He was named Andrew C. Vail Professor in 2010.
Dr. Stanton received the Ussing Award from the American Physiological Society in 2016.
In 2019 Dr. Stanton received the Unsung Hero Award from the Cystic Fibrosis Foundation.
Lung-kidney axis in cystic fibrosis: Early urinary markers of kidney injury correlate with neutrophil activation and worse lung function. Gene expression responses of CF airway epithelial cells exposed to elexacaftor/tezacaftor/ivacaftor suggest benefits beyond improved CFTR channel function. E.PathDash, pathway activation analysis of publicly available pathogen gene expression data. Lung-Kidney Axis in Cystic Fibrosis: Early Urinary Markers of Kidney Injury Correlate with Neutrophil Activation and Worse Lung Function. Gene expression responses of CF airway epithelial cells exposed to elexacaftor/tezacaftor/ivacaftor (ETI) suggest benefits beyond improved CFTR channel function. A Mixed Methods Approach to Understanding the Public Health Impact of a School-Based Citizen Science Program to Reduce Arsenic in Private Well Water. P. aeruginosa tRNA-fMet halves secreted in outer membrane vesicles suppress lung inflammation in cystic fibrosis. P. aeruginosa tRNA-fMet halves secreted in outer membrane vesicles suppress lung inflammation in Cystic Fibrosis. APPLICATION OF QUANTILE DISCRETIZATION AND BAYESIAN NETWORK ANALYSIS TO PUBLICLY AVAILABLE CYSTIC FIBROSIS DATA SETS. Extracellular vesicles secreted by primary human bronchial epithelial cells reduce Pseudomonas aeruginosa burden and inflammation in cystic fibrosis mouse lung. |
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