Robert Lee

What they work on

1. Map how T2R bitter taste receptors in human nasal ciliated cells signal to eNOS, the enzyme that makes nitric oxide, using imaging and biochemistry in primary cells grown at an air-liquid interface.
2. Characterize a newly identified cilia membrane protein that appears to regulate calcium channels in T2R signaling, and test whether its gene variants correlate with symptoms in CF or chronic rhinosinusitis patients.
3. Determine why T2R signaling is reduced in CF cells lacking the CFTR chloride channel, how to restore it to improve bacterial killing, and whether CF modulator drugs alter T2R nitric oxide production.
4. Test how TAS2R38 and TAS2R14 on ciliated cells control mucus clearance and bacterial killing, using Tas2r-deficient and humanized mice challenged with Pseudomonas aeruginosa and sinus inflammation.
5. Determine how the tuft cell receptor TAS2R10 drives IL-25 and acetylcholine release in airway inflammation, using mouse nasal explants, in vivo challenges and single-cell RNA sequencing.
6. Define how T1R sweet receptors in ciliated cells increase glucose transporters to lower airway surface liquid sugar, using cilia-targeted fluorescent biosensors, knockouts and proteomics to identify partner proteins.
7. Test whether TAS1R sweet receptor gene variants and sweet taste intensity predict nasal glucose, Staphylococcus aureus interactions and outcomes, by genotyping and following hundreds of CRS patients.
8. Use tuft-cell-specific fluorescent biosensors in human nasal cultures to learn how tuft cell receptors control calcium, cAMP, electrical excitability and the release of antimicrobial peptides, acetylcholine and IL-25.
9. Define how T2R activation in human macrophages boosts bacterial uptake and killing and dampens toll-like receptor inflammation, and compare macrophages from nasal polyps with blood-derived macrophages from the same patients.

More about the research

Why it matters

Patients with chronic rhinosinusitis, cystic fibrosis, diabetes or asthma face repeated airway infections and inflammation that often resist current treatments. Defining how taste receptors in nasal and immune cells control antimicrobial defenses, airway sugar and inflammation could reveal drug targets. Such drugs might boost natural immunity, for example with bitter compounds or artificial sweeteners. They could reduce reliance on antibiotics and slow the spread of antibiotic resistance.

Known grants

From NIH and NSF research grants. Labs often have other funding we can't see.

Closest labs

The school

University of Pennsylvania: 90 labs on PI Pages, $2.2B a year on research, 750 research doctorates a year.

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