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Erica Herzog, MD, PhD

John Slade Ely Professor of Medicine (Pulmonary) and Professor of Pathology
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Additional Titles

Director, Yale Interstitial Lung Disease (ILD) Center of Excellence, Pulmonary, Critical Care & Sleep Medicine

Associate Dean, Medical Student Research

Contact Info

Pulmonary, Critical Care & Sleep Medicine

PO Box 208057, 300 Cedar Street

New Haven, CT 06520-8057

United States

About

Titles

John Slade Ely Professor of Medicine (Pulmonary) and Professor of Pathology

Director, Yale Interstitial Lung Disease (ILD) Center of Excellence, Pulmonary, Critical Care & Sleep Medicine; Associate Dean, Medical Student Research

Biography

My training as a physician scientist motivates me to seek new treatments for chronic lung diseases. I have spent more than 15 years pursuing this goal by studying the relationship mechanisms of fibrotic remodeling in the adult mammalian lung. My laboratory has had a sustained impact on the field of pulmonary fibrosis and is credited with several seminal discoveries that have been verified and reproduced in laboratories around the world. My early work helped ignite interest in the mechanism(s) through which innate immunity is linked to pulmonary fibrosis. For example, my lab was the first to report that monocytes from patients with Scleroderma associated lung fibrosis adopt profibrotic properties following DAMP stimulation. We reported that the lungs of mice exposed to fibrotic stimuli, and humans with IPF, contain aberrantly activated macrophages that can be repolarized with innate immune agonists to attenuate experimentally induced lung fibrosis. We also are credited with linking intracellular DNA sensors and their ligands with numerous forms of interstitial lung disease. Most recently we reported that a previously unrecognized nerve-lung connection drives mammalian lung fibrosis. My work has been published in journals such as Science, Science Translational Medicine, Nature Medicine, Cell, Journal of Clinical Investigation, Lancet Respiratory Medicine, and the American Journal of Respiratory and Critical Care Medicine. I have been a continuous recipient of NIH funding since 2005 in the form of K08, R01 and U01 awards, and have been honored by my peers with the Jo Rae Wright Award from the American Thoracic Society and induction into the American Society of Clinical Investigation (ASCI). My discoveries in these domains have been informed by collaborations with Yale immunologists, neuroscientists, and bioengineers with the goal of developing new ways to improve respiratory health.

Appointments

Other Departments & Organizations

Education & Training

Clinical Fellow
Yale School of Medicine (2005)
PhD
Yale University School of Medicine (2005)
Resident
Mount Sinai Medical Center, NY (2000)
MD
University of North Carolina at Chapel Hill (1997)
BA
University of North Carolina at Chapel Hill (1993)

Research

Overview

1. Role of the immune system in lung injury, repair, and remodeling. When I embarked upon my PhD during Pulmonary fellowship in 2001, pulmonary fibrosis was viewed as lacking an immunopathogenic component. My graduate work, however, determined that the recruitment and activation of bone marrow derived cells impacts injury, repair, and remodeling via paracrine orchestration of stromal responses. In fact, it was work from my lab, among others, that revitalized interest in how immunity orchestrates fibrotic injury and repair in the adult mammalian lung. We showed that the accumulation of innate immune cells such as macrophages or an ECM producing population of cells called fibrocytes could amplify critical events in fibrogenesis including TGFb1 activation, ECM production, and myofibroblast transformation; that that immune events in the lung could be monitored in the peripheral blood in many forms of human pulmonary fibrosis. We ultimately found that because fibrocytes were rare and difficult to detect in the blood, removal or repolarizing of macrophages is a more viable therapeutic strategy for fibrotic lung disease. These studies have been replicated and expanded by labs around the world and contributed to the preclinical portfolio for the short pentraxin protein PRM151, which recently met its primary endpoint in a Phase II trial.

2. Convergent and divergent mechanisms of injury and repair. Our work has contributed to the growing recognition that cells of the innate immune system display a highly plastic and adaptable phenotype through which they differentially regulate injury and fibrotic remodeling. For example, using the 18-glycolsyl hydrolase protein Chi3L1 as a prototype, we were able to show that a single gene product can simultaneously suppress or promote injury and fibrosis depending on its temporospatial expression in the disease process. We have also shown that danger associated molecular pathogens released by cells exposed to apoptotic, soluble, and mechanical stimuli signal to adjacent cells to initiate a repair program. Importantly, these mediators can be detected in the tissue of patients with various forms of pulmonary fibrosis, cementing the association with human disease. Finally, in very recent work, we have collaborated with investigators in Yale’s School of Immunobiology to describe a new innate immune process by which the inflammation associated hormone GDF15 (also called macrophage inhibitory cytokine 1) controls systemic inflammation and tissue responses via central regulation of peripheral tolerance in multiple organs.

3. Role of Neuronal Guidance Proteins. In delineating the processes described above, we discovered an unexpected contribution of neuronal guidance proteins (NGPs) to IPF and related diseases. In performing these studies we initially focused on NGP function at the so called “immune synapse” through which immune cells communicate. However, as the work has evolved we have observed that NGP function might also relate to their originally described role as regulators of nerve migration and remodeling. Ongoing work in my lab seeks to re-evaluate lung injury, inflammation, pathologic remodeling and repair in the context of macrophage mediated adrenergic nerve remodeling in experimentally induced mammalian lung fibrosis and in IPF.

4. Modeling the Lung Microenvironment. In studying the immune responses described above, we observed that cells that were thought to be terminally differentiated could be reprogrammed by their microenvironment to adopt new functional characteristics. While such an event had been suspected for a while, it became exceedingly evident in our collaboration with Laura Niklason’s lab when cells seeded into a decellularized lungs homed to their geospatial niche, assumed appropriate function, and engendered a living, breathing organ. When we applied this method to fibrotic lungs we observed that the biochemical and biophysical attributes of the lung microenvironment influence the adherence, survival, apoptosis, proliferation, fate specification, and transformation of fibroblasts; and that crosstalk with macrophages influences these endpoints in both animal models and in humans with several forms of lung fibrosis. Our studies revealed a new form of bidirectional feedback between macrophages, fibroblasts, and microenvironmental factors in health and disease that heavily depends upon biophysical cues.

Medical Subject Headings (MeSH)

Bioengineering; Fibrosis; Lung; Lung Diseases, Interstitial; Neuronal Outgrowth; Translational Research, Biomedical

Research at a Glance

Yale Co-Authors

Frequent collaborators of Erica Herzog's published research.

Publications

2024

Clinical Trials

Current Trials

Academic Achievements & Community Involvement

  • honor

    Respiratory Health Recognition Award for Scientific Accomplishments

Clinical Care

Overview

Erica Herzog, MD, PhD, is a pulmonologist who specializes in interstitial lung disease and pulmonary fibrosis. She also cares for patients in Yale New Haven Hospital’s medical intensive care unit.

“I love working with patients to understand their disease, and develop a treatment that aligns with their needs and values,” Dr. Herzog says. “The long-term relationships I have developed with my patients is the most rewarding part of my job.”

Many lung diseases have few effective therapies, and Dr. Herzog tells her patients that physician-scientists are working tirelessly to provide new options. In addition to caring for patients, she is an active researcher herself and is associate dean for medical student research at Yale School of Medicine. “I chose this field to become a respiratory biologist who helps patients breathe more easily,” she says. “As a physician-scientist, I am excited about the opportunity to make a clinical observation in a patient that I then study in the lab. This approach has led to our discovery of new disease mechanisms, many of which are at various stages of clinical development.”

Patients can do their part by exercising, eating right, and being honest about how their doctors can best help them and their families, Dr. Herzog says.

Dr. Herzog is director of Yale's Interstitial Lung Disease Center of Excellence, where she leads a team of physicians, advanced care providers, nurses, support staff, and researchers whose common goal is to provide outstanding care to patients with interstitial lung disease and sarcoidosis, an inflammatory disease that affects the lungs and other organs.

Clinical Specialties

Pulmonology & Sleep Medicine; Pulmonary Critical Care

Fact Sheets

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Get In Touch

Contacts

Academic Office Number
Appointment Number
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Mailing Address

Pulmonary, Critical Care & Sleep Medicine

PO Box 208057, 300 Cedar Street

New Haven, CT 06520-8057

United States

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