Richard I. Enelow, MD
Professor of Medicine
Professor of Microbiology and Immunology
Vice-Chair for Research Affairs, Department of Medicine
Director, Interstitial Lung Disease Program
Microbiology and Immunology
BA Amherst College, 1978
MD Boston University, 1983.
Post-doctoral fellowship, Viral Immunology, University of Virginia, 1992-97
Molecular and Cellular Biology Graduate Programs
1 Medical Center Drive
Lebanon NH 03756
Office: DHMC 5C
Phone: (603) 650-5533
Fax: (603) 650-0580
Assistant: Dana Landis
Asst. Phone: (603) 650-5533
Asst. Email: Dana.R.Landis@hitchcock.org
Immunopathogenesis of respiratory virus infection;
Inflammatory and immune-mediated lung disease
R01AI069360 (PI: Enelow)
"TNF Processing in Pulmonary Immunopathology"
U19 AI83024 (PI: Enelow)
"Innate Regulation of CD8+ T Cell Effector Activities"
Advanced Topics in Immunology
PEMM Immunology Module
My area of research broadly concerns the mechanisms that underlie the immune-mediated damage to the lungs which occurs in the context of respiratory virus infection. My clinical interests include immune-mediated lung disease, particularly the idiopathic interstitial pneumonias, and I have spent my entire career exploring the potential relationship between antiviral T cell responses to respiratory infection to chronic inflammatory lung disease. I became interested in host responses to pulmonary infection as a research fellow in Infectious Disease at the University of Virginia, while pursuing clinical training in Pulmonary Disease. I then spent the next 5 years as a post-doctoral fellow in the laboratory of Dr. Thomas J. Braciale, M.D., Ph.D., (Microbiology/Pathology), Director of the newly-established Beirne B. Carter Center for Immunology Research at the University of Virginia, in order to receive rigorous training in viral immunopathogenesis. Aside from outstanding training and mentoring in addressing questions in basic cellular and molecular immunology, I became fascile with the techniques necessary to work with and manipulate negative-strand RNA viruses, such as influenza and RSV, and these respiratory infections have been the focus of most of my work after moving to Yale, and then to Dartmouth. I have extensive experience in mouse and human basic immunology, and my laboratory is currently home to 2 junior faculty members, 3 postdoctoral fellows, 1 graduate student, and 2 research assistants, so I have ample capacity to take on a variety of collaborative projects in addition to our primary areas of exploration. In addition I have 20 years of experience participating in multi-investigator clinical trials, in interstitial lung disease (particularly idiopathic pulmonary fibrosis), my clinical area of interest, and several publications which have come from these endeavors. For information on the Clinical Research Program in Interstitial Lung Disease see http://www.dartmouth.edu/~renelowlab/the-dartmouth-interstitial.html
Ziritaxestat, a Novel Autotaxin Inhibitor, and Lung Function in Idiopathic Pulmonary Fibrosis: The ISABELA 1 and 2 Randomized Clinical Trials.
Effect of Antimicrobial Therapy on Respiratory Hospitalization or Death in Adults With Idiopathic Pulmonary Fibrosis: The CleanUP-IPF Randomized Clinical Trial.
Single-cell RNA-seq Analysis Reveals That Prenatal Arsenic Exposure Results in Long-term, Adverse Effects on Immune Gene Expression in Response to Influenza A Infection.
STAT2 Signaling Regulates Macrophage Phenotype During Influenza and Bacterial Super-Infection.
Volatile fingerprinting of human respiratory viruses from cell culture.
Infant Infections and Respiratory Symptoms in Relation to in Utero Arsenic Exposure in a U.S. Cohort.
Shedding of TNF receptor 2 by effector CD8⁺ T cells by ADAM17 is important for regulating TNF-α availability during influenza infection.
Influenza-induced type I interferon enhances susceptibility to gram-negative and gram-positive bacterial pneumonia in mice.
The role of IL-27 in susceptibility to post-influenza Staphylococcus aureus pneumonia.
Inflammatory impact of IFN-γ in CD8+ T cell-mediated lung injury is mediated by both Stat1-dependent and -independent pathways.