Selective Myeloid Depletion of Galectin-3 Offers Protection Against Acute and Chronic Lung Injury.

ABSTRACT: Rationale: Galectin-3 (Gal-3) is an immune regulator and an important driver of fibrosis in chronic lung injury, however, its role in acute lung injury (ALI) remains unknown. Previous work has shown that global deletion of galectin-3 reduces collagen deposition in a bleomycin-induced pulmonary fibrosis model (MacKinnon et al., Am. J. Respir. Crit. Care Med., 2012, 185, 537-46). An inhaled Gal-3 inhibitor, GB0139, is undergoing Phase II clinical development for idiopathic pulmonary fibrosis (IPF). This work aims to elucidate the role of Gal-3 in the myeloid and mesenchymal compartment on the development of acute and chronic lung injury. Methods: LgalS3 ^fl/fl mice were generated and crossed with mice expressing the myeloid (LysM) and mesenchymal (Pdg

SUBMITTER: Humphries DC 

PROVIDER: S-EPMC8435800 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature