IL-33 Drives Monocyte Recruitment to Lung Interstitium through Chemokine Upregulation.

ABSTRACT: Tissue infiltration by circulating monocytes is a critical step in the initiation and augmentation of type 2 inflammatory responses in the lungs. Our studies demonstrate that IL-33^-/- mice have a defect in monocyte extravasation from the vasculature to the lung interstitium during induction of type 2 inflammatory responses. This result suggests that monocyte migration to the lungs is IL-33 dependent, and we found that administration of exogenous recombinant IL-33 is sufficient to restore monocyte localization to the lung interstitium. Further investigation of the effect of early administration of recombinant IL-33 on the lungs identified upregulation of multiple chemokines including the monocyte chemoattractants CCL2, CCL7, and CCL22. Importantly, blockade of G-protein coupled r

SUBMITTER: Tjota MY 

PROVIDER: S-EPMC5889047 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature