Deletion of MyD88 in non-parenchymal cells, but not in parenchymal cells attenuates the progression of hepatocellular carcinoma

Increased translocation of intestinal bacteria is a pathological hallmark in patients with chronic liver disease (CLD). Thereby, Toll-like Receptor (TLR) signaling, stimulated by bacterial products, derived from intestinal microbiota, trigger inflammation driving inititation and progression of CLD and hepatocellular carcinoma (HCC). In the current study, the role of MyD88 in parenchymal and non-parenchymal cells in the development of fibrosis and tumour initiation and progression was studied in a murine model of inflammation triggered HCC development.