Small extracellular vesicles from Ptpn1-deficient macrophages alleviate intestinal inflammation by reprogramming macrophage polarization via lactadherin enrichment.

ABSTRACT: Tyrosine-protein phosphatase non-receptor type 1 (Ptpn1) is known to be involved in macrophage polarization. However, whether and how Ptpn1 regulates macrophage phenotype to affect intestinal epithelial barrier function remains largely unexplored. Herein, we investigated the impact of Ptpn1 and macrophage-derived small extracellular vesicles (sEVs) on macrophage-intestinal epithelial cell (IEC) interactions in the context of intestinal inflammation. We found that Ptpn1 knockdown shifts macrophages toward the anti-inflammatory M2 phenotype, thereby promoting intestinal barrier integrity and suppressing inflammatory response in the macrophage-IEC co-culture model. We further revealed that conditioned medium or sEVs isolated from Ptp1b knockdown macrophages are the primary factor driving the

SUBMITTER: Han D 

PROVIDER: S-EPMC9712762 | biostudies-literature | 2022 Dec

REPOSITORIES: biostudies-literature