Stefan Worgall
Weill Medical College of Cornell University, NY·Medicine & Clinical Research
Asthma is the most common chronic lung disease in children. It comes from a mix of genes and outside triggers, especially viral infections.
- Fields
Medicine & Clinical Research
Microbiology & Immunology
Biochemistry
- Topics
asthma
sphingolipids
sphingolipid metabolism
- Grants
- 2 known grants, through Jan 2029
What they work on
- Measure sphingolipid production in children with asthma during and after rhinovirus-triggered asthma attacks, using sphingolipid levels in nasal fluid and blood and gene activity in nasal cells.
- Test how rhinovirus and RSV infection change sphingolipid metabolism in airway lining cells grown at an air-liquid interface, including cells carrying a common 17q21 asthma risk variant.
- Test whether an altered ratio of two sphingolipid signals, sphingosine 1-phosphate and sphinganine 1-phosphate, seen in SPT deficiency and 17q21 risk carriers, causes airway hyperreactivity.
- Determine how SARS-CoV-2 infection affects later respiratory health at different ages in a New York City cohort of children with and without asthma.
- Define epigenetic and gene-activity changes caused by SARS-CoV-2 in blood-forming stem cells, and test how asthma risk variants shape nasal-cell responses to SARS-CoV-2 followed by RSV or rhinovirus.
More about the research
A common risk region of DNA, 17q21, contains the gene ORMDL3. This gene controls an enzyme called serine-palmitoyl CoA transferase (SPT), which starts the production of sphingolipids. Sphingolipids are fats that help build cell membranes and act as signals. The lab's two projects ask how this genetic change in sphingolipid production shapes asthma and children's responses to respiratory viruses, including SARS-CoV-2, the virus that causes COVID-19.
Why it matters
Many children carry asthma risk genes that change sphingolipid production. Showing how rhinovirus, the main trigger of asthma attacks, affects these fats could point to new asthma treatments that target sphingolipid metabolism. Learning how SARS-CoV-2 changes children's later responses to colds and reinfection could guide care for children with asthma. This is especially relevant for families from communities with high exposure and health disparities.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Anny Zhou
University of Virginia, VA·Microbiology & Immunology
Dissect the molecular mechanism by which GSDMB, an asthma-linked gene on chromosome 17q21, promotes interferon signaling and the expression of interferon-stimulated genes in human airway epithelial cells treated with RNA viruses or the viral RNA mimic poly(I:C).
Jennifer Melinda Bomberger
Dartmouth College, NH·Microbiology & Immunology
Test whether TsiT, a T6SS immunity protein that resembles LysR-type gene regulators, acts as a transcriptional regulator that controls Pseudomonas aeruginosa biofilm formation.
Stefanka Spassieva
University of Kentucky, KY·Neuroscience
Test whether high brain levels of sphingoid bases and their phosphates in CerS1-deficient mice change gene activity in neurons and glia over time, disrupting neuronal maturation and differentiation.
The school
Weill Medical College of Cornell University: 35 labs on PI Pages, $1.6B a year on research, 59 research doctorates a year.
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