division of pulmonary, critical care & sleep medicine
Bryant Lab
research

Andrew J. Bryant, MD
Associate Professor of Medicine (tenured)
andrew.bryant@medicine.ufl.edu
Overview
The Bryant Lab studies the role of myeloid-derived immunoregulatory cells in the development of pulmonary hypertension, utilizing preclinical (small animal) models and clinical/translational studies. The laboratory focus is regulation of these innate immune cells via circadian rhythms, STING-signaling, and the central nervous system.
Focus Areas
- Pulmonary Hypertension
- Circadian Biology
- Myeloid-Derived Suppressor Cells
- STING-Mediated Inflammatory Signaling
- Brain-Lung Axis Signaling
Lab Staff
Biological Scientist
Chunhua Fu
- The Bryant Lab is inclusive and welcomes inquiries from postdoctoral fellows, and graduate and undergraduate students interested in translational research in pulmonary vascular disease. If you are interested, please reach out to the PI, Dr. Andrew Bryant.
publication highlights
- Morning Larks and Night Owls: Considering Chronotype in Evaluation of Patients with Pulmonary Hypertension
- Opposing roles for myeloid and smooth muscle cell STING in pulmonary hypertension
- The common Sting1 HAQ, AQ alleles rescue CD4 T cellpenia, restore T-regs, and prevent SAVI (N153S) inflammatory disease in mice
- Non-Interferon-Dependent Role of STING Signaling in Pulmonary Hypertension
- Defining the age-dependent and tissue-specific circadian transcriptome in male mice
- A wrinkle in time: circadian biology in pulmonary vascular health and disease
- The Third Man: DNA sensing as espionage in pulmonary vascular health and disease
- Emergency myelopoiesis contributes to immune cell exhaustion and pulmonary vascular remodelling
- Chemokine signaling axis between endothelial and myeloid cells regulates development of pulmonary hypertension associated with pulmonary fibrosis and hypoxia
- Myeloid-derived Suppressor Cells Are Necessary for Development of Pulmonary Hypertension
For more PI Publications please follow the links below

