Therapeutic targeting of adipose tissue macrophages ameliorates liver fibrosis in non-alcoholic fatty liver disease

Background and aimsThe accumulation of adipose tissue macrophages (ATMs) in obesity has been associated with hepatic injury. However, the ATMs contribution to fibrosis non-alcoholic fatty liver disease (NAFLD) remains be elucidated. Herein, we investigate relationship between NAFLD patients evaluate impact modulation over an experimental NASH model.MethodsAdipose biopsies from 42 different stages were collected. characterized by immunohistochemistry flow cytometry correlation was assessed. Selective phenotype achieved ip administration dextran coupled dexamethasone diet induced obese murine models. Chronic effects evaluated histology gene expression analysis samples. In vitro crosstalk human stellate cells (HSC) spheroids performed.ResultsNAFLD presented increased pro-inflammatory that correlated fibrosis. Long term significantly reduced ameliorated inflammation. Moreover, improvement steatosis inflammation progression model. vitro, reduction dextran-dexamethasone treatment secretion inflammatory chemokines directly attenuated pro-fibrogenic response HSC spheroids.ConclusionsPro-inflammatory increase parallel degree their model improves fibrosis, uncovering potential as a therapeutic target mitigate NAFLD.Impact implicationsWe report correlate NAFLD. Furthermore, dextran-nanocarrier conjugated shifts ATM anti-inflammatory NASH. This shift ameliorates inflammation, Our results highlight relevance pathophysiology unveil for