Airway epithelium-shifted mast cell infiltration regulates asthmatic inflammation via IL-33 signaling.

ABSTRACT: Asthma is a heterogeneous syndrome that has been subdivided into physiologic phenotypes and molecular endotypes. The most specific phenotypic manifestation of asthma is indirect airway hyperresponsiveness (AHR), and a prominent molecular endotype is the presence of type 2 inflammation. The underlying basis for type 2 inflammation and its relationship to AHR are incompletely understood. We assessed the expression of type 2 cytokines in the airways of subjects with and without asthma who were extensively characterized for AHR. Using quantitative morphometry of the airway wall, we identified a shift in mast cells from the submucosa to the airway epithelium specifically associated with both type 2 inflammation and indirect AHR. Using ex vivo modeling of primary airway epithelial cells in organ

SUBMITTER: Altman MC 

PROVIDER: S-EPMC6819127 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature