Investigators demonstrated that PTGIS was downregulated in alchoholic liver disease and forced PTGIS expression in vivo using recombinant adeno-associated viral vector-packed prostacyclin synthase overexpression plasmid, which alleviated the inflammatory response and suppressed the macrophage M1 phenotype in mice.
Scientists review the roles of multiple immunological mechanisms and therapeutic targets related to the inflammation associated with fatty liver diseases and the differences in the progression of alcoholic liver disease and nonalcoholic fatty liver disease. Multiple cell types in the liver, including macrophages, neutrophils, other immune cell types and hepatocytes, are involved in fatty liver disease inflammation.
Currently, neutrophils, with their autocrine, paracrine, and immune modulation functions, have been shown to be involved in liver diseases, including viral hepatitis, nonalcoholic steatohepatitis, alcoholic liver disease, liver fibrosis, cirrhosis, liver failure, and liver cancer. Accordingly, this review summarizes the role of neutrophils in liver diseases.