Table 1.

Monocyte-macrophages display pro- and anti-inflammatory phenotypes in end-stage liver disease.

Anti-inflammatory phenotype		Pro-inflammatory phenotype
Monocyte-Macrophage:		Monocyte-Macrophage:
Rimola et al. (10)	In vivo: Decreased reticuloendothelial system phagocytosis in cirrhosis (DC) compared to HC, by tracer elimination method. This was associated with increased incidence of bacterial infection.	Albillos et al. (11)	Ex vivo: Increased activation markers (HLA-DR and CD80) and intracytoplasmic TNFα expression in monocytes from cirrhosis (DC) compared to HC.
Gomez et al. (12)	In vivo: Decreased macrophage-mediated clearance of IgG-coated erythrocytes in cirrhosis (mixed SC and DC). This was associated with increased incidence of bacterial infection.	Tazi et al. (13)	Ex vivo: Greater increase in LPS-induced monocyte TLR4 expression and TNFα release from cirrhotic patients compared to HC.
Wasmuth et al. (14)	Ex vivo: Decreased monocyte LPS-induced TNFα production and HLA-DR expression in ACLF compared to SC.	Gandoura et al. (15)	Ex vivo: Microarray gene expression profiling of PBMCs from ARLD cirrhosis (DC) showed decreased induction of type-1 and type-2 IFN-stimulated genes, compared to HC (see left column).
Gandoura et al. (15)	Ex vivo: Microarray gene expression profiling of PBMCs from ARLD cirrhosis (DC) compared to HC, showed increased induction of pro-inflammatory cytokine genes (IL-6, IL-8, TNFα), but decreased induction of type-1 and type-2 IFN-stimulated genes, compared to HC (see right column).
O'Brien et al. (16)	Ex vivo: Plasma from DC and ACLF led to decreased LPS-stimulated TNFα release and bacterial killing when incubated with healthy monocyte-macrophages, compared to plasma from stable cirrhosis.
Bernsmeier et al. (17)	Ex vivo: Decreased monocyte LPS-induced TNFα and IL-6 production in DC and ACLF compared to stable cirrhosis. No change in ROS production.