January 2016 (Discovery Medicine)
“Taken together, our results demonstrate that infiltrating monocytes may play a pathological role in exacerbating chronic liver inflammation and fibrosis in CLD. MCP-1 may be involved in the monocyte infiltration and progression of liver inflammation and fibrosis in CLD.Chronic liver diseases (CLD) are major health problems. Patients with CLD independent of its origin are prone to develop liver fibrosis and cirrhosis, which may result in potentially lethal complications such as hepatic decompensation and hepatocellular carcinoma (Tsochatzis et al., 2014).
Although liver fibrosis with different etiologies (e.g., chronic viral hepatitis, alcohol abuse and autoimmune disorders) employs different mechanisms of hepatocyte injury, the resulting steps promoting fibrosis development are astonishingly similar (Heymann et al., 2009). Inflammation is considered to be the key factor of the initiation and maintenance of fibrotic processes in the liver (Iredale, 2007; Karlmark et al., 2008). Persistent hepatic inflammation may promote the apoptosis of parenchymal cells and replacement by connective tissue and extracellular matrix (ECM) proteins. Hepatic stellate cell (HSC) activation is the key step for liver fibrogenesis through producing a large amount of ECM proteins.
However, over recent years, several studies have emphasized the crucial role of hepatic macrophages for the progression of liver inflammation and fibrosis in experimental mouse models (Baeck et al., 2012; 2014; Duffield et al., 2005; Heymann et al., 2012; Karlmark et al., 2009).”