About

Lisa R. Young, M.D., is a Professor of Pediatrics (Pulmonary Medicine) at the Perelman School of Medicine at the University of Pennsylvania. She serves as the Associate Director of the Penn-CHOP Lung Biology Institute at Children's Hospital of Philadelphia and the University of Pennsylvania. Dr. Young is also a Senior Advisor and a member of the Chief Scientific Officer Leadership Team at the Children's Hospital of Philadelphia Research Institute. Her research focuses on pulmonary biology, including lung alveolar epithelial cell inflammation, neuroendocrine cell hyperplasia, pulmonary fibrosis susceptibility, and childhood interstitial lung diseases. She has contributed to understanding the molecular mechanisms underlying lung diseases and has published extensively on topics related to pulmonary health and disease.

Research topics

• Political Science
• Business
• Sociology
• Medicine
• Family medicine
• Marketing
• Environmental health
• Engineering
• Management
• Medical education
• Food science
• Biology
• Nursing
• Public relations

Selected publications

• Reporting ABCD1 variants as actionable secondary findings on exome and genome sequencing

  Genetics in Medicine · 2025-04-07

  editorialOpen access
  PublisherOA PDFDOI

• Spatial and Temporal Assessment of Cerebral Blood Flow in a Novel Piglet Model of Neonatal Arterial Ischemic Stroke

  Research Square · 2025-09-01

  preprintOpen access
  PublisherOA PDFDOI

• Hermansky-Pudlak Syndrome

  Clinics in Chest Medicine · 2025-09-01 · 1 citations

  reviewSenior author
  PublisherDOI

• Associations of Traumatic Brain Injury and Mild Behavioral Impairment With Cognitive Function and Dementia

  Journal of Geriatric Psychiatry and Neurology · 2025-01-30 · 1 citations

  article

  ObjectiveTraumatic Brain Injury (TBI) may contribute additional complexity to the clinical picture of mild behavioral impairment (MBI). MBI, a behavioral analog to mild cognitive impairment (MCI), is comprised of five neuropsychiatric domains: decreased motivation, affective dysregulation, impulse dyscontrol, social inappropriateness, and abnormal perception/thought content. We investigated (1) if cross-sectional associations of cognitive status with MBI symptoms differ by TBI status and (2) if prospective associations of MBI domain positivity with incident dementia risk differ by TBI status.Methods2246 participants without dementia from the Atherosclerosis Risk in Communities Study were included (mean age = 75.6 years, 59.0% female). TBI was defined by self-report/ICD-9/10 codes, MBI via an established algorithm based on the Neuropsychiatric Inventory Questionnaire, and baseline cognitive status/incident dementia using neuropsychological tests, informant interviews, and hospital/death certificate codes.ResultsCross-sectionally, although MCI status was associated with greater odds of MBI, this did not differ based on TBI status (MCI with TBI: OR = 2.04, 95% CI = 1.44-2.88, MCI without TBI: OR = 1.60, 95% CI = 1.20-2.14). Individuals with MCI (with or without TBI) were more likely to have decreased motivation, affective dysregulation, and impulse dyscontrol. Prospectively, positivity in 1+ MBI domains was associated with increased risk of incident dementia, not differing by TBI status (no TBI and MBI: HR = 2.15, 95% CI = 1.55-2.99, TBI and MBI: HR = 2.62, 95% CI = 1.81-3.80).ConclusionsNeither cross-sectional associations between cognitive status and MBI domain positivity nor prospective associations of MBI domain positivity with incident dementia risk differed by TBI status. How TBI may relate to neuropsychiatric symptomatology in the context of neurodegenerative processes requires further clarification.

  PublisherDOI

• Dietary saturated fatty acids promote lung myeloid cell inflammasome activation and IL-1β–mediated inflammation in mice and humans

  Science Translational Medicine · 2025-08-27 · 5 citations

  articleOpen access

  Resident tissue macrophages and monocytes (RTMs) integrate local and systemic signals to coordinate immune cell function at homeostasis and in response to inflammatory stimuli. Obesity-associated metabolic dysfunction drives the development of RTM populations that contribute to disease states in multiple tissues. However, the contribution of specific dietary components to innate immune cell activation and function, as opposed to the direct effects of obesity, is largely unknown. Here, we studied the mechanisms by which high-fat (HF) diets shape lung RTM phenotype and function at steady state and influence responses to inflammatory insults. We found that, during HF diet feeding, lung RTMs accumulate saturated long-chain fatty acids, specifically stearic acid (SA), and demonstrate features of NLRP3 inflammasome priming and activation. In vivo, increased dietary SA was sufficient to cause neutrophil-predominant lung inflammation in the steady state and exacerbate a model of innate airway inflammation, whereas increased dietary oleic acid, the monounsaturated counterpart of SA, was sufficient to reduce inflammasome activation in the steady state and attenuate airway inflammation. Depletion of interleukin-1β (IL-1β) or pharmacologic inhibition of the endonuclease inositol requiring enzyme 1α (IRE1α) protected against SA-induced exacerbated lung inflammation. Last, we identified a population of lung monocytes with hallmarks of HF diet-induced RTM activation that were present in samples from obese humans with asthma. Together, these results identify a class of dietary lipids that regulate lung RTM phenotype and function in the steady state and modulate the severity of inflammation in the lung.

  PublisherOA PDFDOI

• Management of severe acute pulmonary haemorrhage in children

  The Lancet Child & Adolescent Health · 2025-04-15 · 5 citations

  reviewOpen access
  PublisherOA PDFDOI

• P225: Implementing genetic testing and counseling in a rare lung diseases clinic at a pediatric tertiary care center

  Genetics in Medicine Open · 2025-01-01

  articleOpen accessSenior author
  PublisherDOI

• Abnormal Baseline Pulmonary Status Before Hematopoietic Stem Cell Transplant is Underrecognized: A Report from the Transpire Study

  American Journal of Respiratory and Critical Care Medicine · 2025-05-01

  article

  Abstract Background: Poor lung function before allogeneic hematopoietic stem cell transplant (all-HSCT) is a significant cause of post-transplant pulmonary complications and mortality. TRANSPIRE is a currently enrolling multi-institutional study examining pulmonary injury in a prospective cohort of pediatric and young-adult patients receiving allo-HSCT. Methods: Patients enrolled in TRANSPIRE (a 7 site prospective cohort study of pediatric and young adult allo-HSCT patients) underwent uniform pre-BMT testing with pulmonary function testing (PFT) (spirometry, plethysmography, diffusing capacity, 6-minute walk test (6MWT)), chest computed tomography (CT) scan, and bronchoscopy with bronchoalveolar lavage (BAL) if clinically indicated. Test results and clinical history were reviewed by the local pulmonologist to classify each patient as having normal or abnormal baseline pulmonary status. Results: We analyzed 168 patients undergoing HSCT who were categorized based on their baseline pulmonary status: 101 patients (60%) with abnormal pulmonary status and 67 patients (40%) with normal pulmonary status. Patient characteristics are further described in Table 1. The distribution of sex did not significantly differ between the groups (p=0.53). Patients with abnormal pulmonary status were significantly older, with a median age of transplant of 13.4 years (IQR 9.2 to 17.5). In the abnormal pulmonary status group, malignancy was and immune deficiency were more frequent indications for HSCT with all children with immune deficiency being assessed as abnormal. Aggregate PFT xparameters did not differ between patients with abnormal and normal lung function at baseline (Table 1) although the most common reason for an abnormal pulmonary baseline determination was PFT abnormalities (n=79, 78.2%) (Table 2). Conclusions: We observed a high frequency of patients undergoing HSCT who had abnormal pulmonary status at baseline with a majority of cases assessed as abnormal. These data emphasize the need for careful evaluation of pulmonary status in children proceeding to transplantation and early referral to a pulmonologist, particularly in children with immune deficiency or malignancy as the indication for HSCT.

  PublisherDOI

• Upper and lower airway microbiota across infancy and childhood

  Pediatric Research · 2025-03-12 · 6 citations

  articleOpen access

  BACKGROUND: The upper and lower respiratory tracts feature distinct environments and responses affecting microbial colonization but investigating the relationship between them is technically challenging. We aimed to identify relationships between taxa colonizing the nasopharynx and trachea across childhood. METHODS: We employed V4 16S rRNA gene sequencing to profile nasopharyngeal swabs and tracheal aspirates collected from 172 subjects between 20 weeks and 18 years of age. These samples were collected prior to elective procedures over the course of 20 weeks in 2020 from subjects enrolled in a cross-sectional study. After extraction, sequencing, and quality control, we studied the remaining 147 of 172 nasopharyngeal swabs and 95 of 172 tracheal aspirates, including 80 subject-matched pairs of samples. RESULTS: Sequencing data revealed that the nasopharynx is colonized by few, often highly abundant taxa, while the tracheal aspirates feature greater diversity. The patterns of colonization identified in the nasopharynx correlate with subject age across childhood. CONCLUSION: Our data suggests that there are relatively few species that colonize both the nasopharyngeal tract and the trachea. Furthermore, we observe a pattern of change in the nasopharyngeal microbiota that is correlated with age, suggesting a possible developmental progression of the nasopharyngeal microbiota across childhood. IMPACT: The airway microbiota in childhood plays important roles in respiratory health and immune development. In this work, we report on paired nasopharyngeal swab and tracheal aspirate samples from a cross-sectional cohort of children from infancy to 18 years. We find that the upper and lower airway microbiota are unlikely to share taxa and do not correlate in terms of diversity. We show that the composition of the upper airway microbiota is strongly correlated with age, with a stereotypic developmental trajectory during childhood and adolescence. Our results inform our understanding of airway microbiota assembly and may be used to predict airway disease in young children.

  PublisherOA PDFDOI

• Genetic Testing Utilization in the U.S. Registry for Childhood Interstitial and Diffuse Lung Diseases

  Pediatric Pulmonology · 2025-04-01 · 5 citations

  articleOpen accessCorresponding

  INTRODUCTION: Childhood interstitial and diffuse lung diseases (chILD) comprise a diverse group of rare disorders. Identifying the underlying cause is crucial for treatment, prognosis, and estimating recurrence risk. The objective of this study was to assess the utilization of genetic testing for subjects enrolled in the United States National Registry for ChILD, a multicenter observational study. METHODS: Genetic data from participating sites were reviewed and analyzed in relationship to clinical characteristics. RESULTS: Of 609 children enrolled from 22 centers, genetic testing was performed for 55.5% (n = 338). Genetic testing results were positive (diagnostic) for 22.8% (n = 77), negative for 60.7% (n = 205), and uncertain for 16.6% (n = 56). Most testing was performed through gene panels (55.9%), followed by exome sequencing (ES) or whole genome sequencing (WGS) (26.9%), single gene testing (24.6%), and/or chromosomal microarray (11.8%). For participants with positive (diagnostic) genetic testing results, the majority were diagnosed through gene panel (33.8%; n = 26) or single gene testing (32.5%; n = 25). The most common diagnosis confirmed by genetic testing was SFTPC-associated surfactant metabolism dysfunction. Of the 59 subjects with unclassified ILD, only 22% (n = 13) had undergone ES or WGS, 61% (n = 36) had received panel testing, and 27% (n = 16) did not have any genetic testing reported. CONCLUSION: The utilization of genetic testing has been variable in infants and children enrolled in the ChILD Registry. Additional efforts are needed to develop genetic testing recommendations for children with suspected ILD. Furthermore, there is opportunity for broader utilization of ES/WGS and genetic discovery for children with lung disease of unclear etiology.

  PublisherOA PDFDOI

Recent grants

• Midcareer Investigator Award in Patient-Oriented Research in Pediatric Rare Lung Diseases

  NIH · $540k · 2019–2024

• NIH Grant K08HL082757

  NIH · $640k · 2013

• Mechanisms of Pulmonary Fibrosis in Hermansky-Pudlak Syndrome

  NIH · $3.6M · 2013–2024

Frequent coauthors

• Robin R. Deterding

  76 shared

• Gail Deutsch

  Seattle Children's Hospital

  70 shared

• Francis X. McCormack

  University of Cincinnati

  60 shared

• Lynn Buckley

  East Riding of Yorkshire Council

  49 shared

• Nafisa Patel

  Leicester Royal Infirmary

  49 shared

• H. Manderville

  University Hospital Coventry

  49 shared

• Sandeep K. Chahal

  University of Glasgow

  49 shared

• Laura Appadu

  Royal Marsden Hospital

  49 shared

Labs

• Lisa R. Young LabPI