Why can inflammatory programs persist after molecular correction?
We examine residual inflammatory states in human disease using molecular profiling anchored to clinical phenotype.
From clinical phenotype to molecular mechanism.
We integrate patient-derived samples with lipidomics, metabolomics and experimental biology to investigate inflammation, resolution and clinically meaningful molecular states.
Omics are not the endpoint. They are a way to connect what we measure in patients with the biology that drives disease.
Profiling lipid mediator networks that accompany initiation, persistence and resolution of inflammation.
02MetabolomicsMapping metabolite signatures in patient-derived samples and linking them to defined clinical phenotypes.
03TranslationIntegrating molecular readouts with pharmacology and experimental models to build testable biological hypotheses.
Our workflow starts with a precise clinical question, not with a technology. Samples, analytical platforms and experimental systems are selected around the biological problem.
Patients, phenotype and the clinical question.
Lipidomic, metabolomic and complementary molecular readouts.
Molecular features with clinical and inflammatory phenotypes.
Mechanisms that can be challenged experimentally.
We examine residual inflammatory states in human disease using molecular profiling anchored to clinical phenotype.
We study how airway-proximal pharmacology can inform treatment response and clinical biology.
The laboratory works at the interface of human samples, analytical chemistry and experimental biology, with the aim of turning molecular signatures into biologically testable questions.