Levy Research Group

Dr. Levy is trained in both pediatric and adult medicine. Her clinical interests include cystic fibrosis, transition from pediatric to adult care, and diagnostic dilemmas.

After her undergraduate studies at Stanford University, Levy earned her MD at the Medical College of Wisconsin and her Master of Medical Sciences at Harvard Medical School. She completed her clinical fellowship in Pulmonary Medicine at Children’s Hospital Boston and prior to fellowship her residency in Internal Medicine and Pediatrics at the Medical College of Wisconsin.

In addition to treating patients, Levy’s work at the University of Wisconsin School of Medicine and Public Health include translational research into the cellular and molecular underpinnings of clinical heterogeneity and response to airway infection in cystic fibrosis. Specifically, Levy’s research investigates how immune responses in persons with cystic fibrosis may be epigenetically modified with exposure to airway infection.  Her lab uses multiple in vitro approaches to dissect the genetic and epigenetic components of defining the immune response and possible dysregulation with the goal of more precisely defining a cystic fibrosis patient’s clinical course and treatment response. She spearheads several research projects and has co-authored more than 35 peer-reviewed publications.

Research Highlight

Project title: Enriching CF Newborn Screening Outcomes through a Precision Personalized Medicine Strategy

Epidemiological studies provide a foundation for Dr. Levy’s  research funded by the Rosenau Family Research Foundation to explore the epigenomic underpinnings that contribute to clinical outcomes among children with cystic fibrosis (CF). The aim of this work is to relate molecular signatures to CF-NBS implementation and expect our research to enhance understanding, diagnosis, and targeted treatment of CF respiratory infections and their complications, with potential applications to other chronic airway conditions.

Significant advances in early diagnosis through newborn screening (NBS) and genotype characterization have greatly enhanced the quality of life for children with CF. However, underrepresented populations have not benefitted equally from these advancements, nor have White patients for reasons that are unknown. Notably, while CF has traditionally been perceived as a disease predominantly affecting White individuals, recent evidence indicates that approximately 20% of NBS-diagnosed cases in the U.S. occur in African American, Hispanic, and other minority populations. Unfortunately, these groups face disparities, including significant delays in diagnosis — often being older at the time of their first evaluation at CF care centers compared to White infants — and poorer treatment outcomes, such as more frequent pulmonary exacerbations at a young age.

Moreover, patients from minoritized backgrounds are more likely to have unidentified CFTR mutations, even though 75-80% of those eligible for treatment with CFTR modulators are from these populations. This highlights the need for NBS to incorporate additional components to identify patients with CF who are not detected by standard screening for CFTR mutations. 

Inspired by the Wisconsin NBS Project, our research investigates the molecular basis for disparate pulmonary outcomes in children with CF, specifically focusing on Pseudomonas aeruginosa (Pa) respiratory infections. Our previous studies have shown that children with CF exhibit changes in inflammation-related transcripts correlating with disease status. We, along with others, have identified impairments in monocyte and macrophage functions in CF, which are not corrected by CFTR modulators. While most research has concentrated on genetic mutations and epigenetic modifications, few studies have explored how differential gene expression profiles may affect susceptibility to respiratory diseases. Using CF airway infections as a model system we will uncover fundamental pathways that impact lung immune responses and potential targets for therapeutic intervention.