Leaders from the Department of Pediatric Newborn Medicine at Brigham and Women’s Hospital had a strong presence at the Pediatric Academic Societies’ annual 2022 meeting, which took place April 21 – 25, 2022, in Denver, CO.
This year’s event was well-attended, with over 6,300 people representing 53 countries and 70 specialties. Dozens of Brigham faculty attended this year’s event, presenting their latest research to international experts via poster sessions, oral abstract presentations, panel discussions, and more throughout the conference.
Highlighted Brigham Presentations
The Maternal-Infant Dyad and Cardiometabolic Health
Mandy Brown Belfort, MD, MPH, Associate Professor of Pediatrics and Director of Clinical Research
As part of a group session titled, “Preterm Birth and the Life Course: Implications for NICU Follow-through Care,” Dr. Belfort presented research indicating that former preterm infants are at an increased cardiometabolic risk compared to full-term infants, including a higher risk of diabetes, ischemic heart disease, stroke, and more. These risks emerge from exposures early in the lifecourse during the prenatal, NICU, and post-discharge periods. Dr. Belfort discussed how cardiometabolic screening and preventative measures might fit into current models of NICU follow-up. Further research is required to inform implementation, including research to determine the effectiveness of such approaches, and the roles of primary care, subspecialty, and community-based providers in relation to NICU follow-up.
Role and Regulation of Autophagy in Bronchopulmonary Dysplasia
Sule U. Cataltepe, MD, Medical Director of Newborn Respiratory Care
Bronchopulmonary dysplasia (BPD) is a common and serious pulmonary morbidity associated with prematurity. Dr. Cataltepe presented a recently published study in the American Journal of Respiratory Cell and Molecular Biology and unpublished data from her NIH-funded laboratory that explored the role of autophagy—a highly conserved and regulated lysosomal degradation pathway that maintains cellular homeostasis—in BPD. Using murine and non-human primate models of BPD, Dr. Cataltepe and colleagues found that autophagy is impaired during the evolution of BPD. The augmentation of autophagy with a pharmacologic activator of 5′-AMP–activated protein kinase (AMPK) protected against BPD in the murine model. Collectively, these studies suggest that the AMPK-autophagy pathway can be leveraged to develop novel therapeutics for BPD.
Role of Autophagy in Sepsis and Resolution of Inflammation
Sailaja Ghanta, MD, Attending Neonatologist
Despite intense efforts to improve the early diagnosis and treatment of neonatal sepsis, mortality and morbidity from this common condition remain high. Dr. Ghanta presented her work investigating approaches using mesenchymal stromal cells (MSCs) as a therapy to eradicate the infection, resolve the inflammatory response, protect organs from injury, and improve sepsis survival in infants. She presented results linking autophagy in MSCs and host resolution of inflammation. The long-term goal is to modulate autophagy to optimize MSC treatment for the devastating disease of sepsis.
Maternal Pre-Pregnancy Obesity Drives a Specific Placental Transcriptome Signature That Is Associated With Newborn Fat Mass at Birth: A Case-Control Study
Carmen Monthé-Drèze, MD, Director, Physician Well-Being
Pre-pregnancy obesity is linked to excessive in utero adiposity accrual in the offspring, which is associated with later obesity and type 2 diabetes. The mechanisms underlying these links have been understudied, and the goal of this investigation was to identify molecular pathways to explain these observations. Dr. Monthé-Drèze and colleagues performed targeted transcriptomic analysis of placentae of newborns with high vs. low adiposity born to mothers with either obesity or normal weight. The investigators found broad-scale upregulation of placental metabolic pathways in the highest (vs. lowest) offspring adiposity group, specifically among placentae of women with obesity. Additionally, they identified that distinct placental biological pathways and unique placental genes may underpin fetal fat mass accrual in pregnancies complicated by maternal obesity. However, adiposity among newborns of women with normal weight was not explained by a distinct transcriptomic signature. Findings could inform therapeutic targets for one in three dyads in the U.S. to interrupt intergenerational obesity.