I’m a neonatologist and researcher seeking to understand lung development and repair after neonatal injury in preterm infants. Through my clinical and research activities, I hope to develop a comprehensive program of care for extremely premature infants that minimizes the risk of severe bronchopulmonary dysplasia (BPD) and optimizes lung development and function.
During my fellowship training in neonatal-perinatal medicine, I began conducting basic-translational research that evaluated the role of matricellular proteins in saccular and early alveolar lung development. My colleagues and I determined that hyperoxia exposure resulted in misexpression of the Transforming Growth Factor Beta (TGFβ)-responsive extracellular matrix proteins, periostin and TGFBI, during critical periods of saccular-alveolar lung development.
Periostin proved to be a novel marker for both normal myofibroblastic activity during alveolarization and abnormal myofibroblastic persistence during late fibrotic stages of lung injury. Additionally, TGFBI proved to be another early, robust marker of dysregulated interstitial fibroblast function in the early phase of lung injury and the late phases of repair.
I’ve recently transitioned my focus and attention away from the basic laboratory toward understanding clinical indicators of early lung injury. As part of a scholar grant through the Prematurity and Respiratory Outcomes Program (PROP), I helped demonstrate for the first time that plasma periostin levels in extremely premature infants during the first weeks of life correlate with the development and severity of BPD.
Ongoing efforts to understand periostin's role as an early biomarker of persistent lung injury — potentially identifying patients that would benefit from systemic steroids — are underway. Additionally, we’re conducting studies to identify clinical factors that may predict response to late systemic steroid use in infants with severe, established BPD. These efforts and others are designed to individualize therapy and understand the responsiveness of adjunctive medications commonly used to manage severe BPD.
Our future research efforts will focus on understanding early factors associated with the development of severe BPD, identifying early interventions that can modulate BPD severity and defining responsiveness to commonly used but variably effective adjunctive medications (including diuretics, inhaled corticosteroids and bronchodilators).
In my role as a clinician, I serve on both the Cincinnati Children’s Perinatal Institute BPD Quality Improvement and BPD Center of Excellence Clinical Care teams. These teams aim to optimize the prevention and treatment of BPD.
MD: Indiana University School of Medicine, Indianapolis, IN, 2005.
Residency: Pediatrics, James Whitcomb Riley Hospital for Children, Indiana University School of Medicine, Indianapolis, IN.
Fellowship: Neonatal-Perinatal Medicine, James Whitcomb Riley Hospital for Children, Indiana University School of Medicine, Indianapolis, IN.
Certification: General Pediatrics, 2008; Neonatal and Perinatal Medicine, 2012.
Neonatal-perinatal medicine; bronchopulmonary dysplasia
Neonatology, Perinatal, Fetal Care, Newborn Intensive Care NICU, Bronchopulmonary Dysplasia BPD
Neonatal lung injury, development, and repair; neonatal lung mesenchymal development; biomarkers of neonatal lung injury; animal models of bronchopulmonary dysplasia
Neonatology, Perinatal Biology, Pulmonary Biology, Developmental Biology
Tracheostomy prediction model in neonatal bronchopulmonary dysplasia via lung and airway MRI. Pediatric Pulmonology. 2022; 57:1042-1050.
Cover Image, Volume 57, Number 4, April 2022. Pediatric pulmonology. Supplement. 2022; 57:ii-ii.
Maladaptive functional changes in alveolar fibroblasts due to perinatal hyperoxia impair epithelial differentiation. JCI insight. 2022; 7.
Safety of sildenafil in extremely premature infants: a phase I trial. Journal of Perinatology. 2022; 42:31-36.
Morbidity and respiratory outcomes in infants requiring tracheostomy for severe bronchopulmonary dysplasia. Pediatric Pulmonology. 2021; 56:2589-2596.
Insulin-like Growth Factor 1 Supports a Pulmonary Niche that Promotes Type 3 Innate Lymphoid Cell Development in Newborn Lungs. Immunity. 2020; 52:275-294.e9.
Neonatal Lung Disease Associated with TBX4 Mutations. Journal of Pediatrics. 2019; 206:286-292.e1.
Neonatal hyperoxia promotes asthma-like features through IL-33-dependent ILC2 responses. Journal of Allergy and Clinical Immunology. 2018; 142:1100-1112.
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