Residual inflammation
Which inflammatory states persist despite effective CFTR modulation?
Residual airway inflammation and resolution biology in the era of CFTR modulators.
Highly effective CFTR modulators have transformed cystic fibrosis care, but molecular correction does not necessarily erase every downstream inflammatory program. We study residual airway inflammation using patient-derived samples, clinical phenotyping and molecular profiling.
Which inflammatory states persist despite effective CFTR modulation?
Are pro-resolving lipid pathways restored, incompletely engaged or uncoupled from clinical improvement?
Why do people receiving the same therapy show different molecular and clinical responses?