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The expression of chemokine receptor CX 3 CR1 is related to migration and signaling in cells of the monocyte-macrophage lineage. The precise roles of CX 3 CR1 in the liver have been investigated but not clearly elucidated. Here, we investigated the roles of CX 3 CR1 in hepatic macrophages and liver injury. Hepatic and splenic CX 3 CR1 low F4/80 low  monocytes and CX 3 CR1 low CD16 −  monocytes were differentiated into CX 3 CR1 high F4/80 high  or CX 3 CR1 high CD16 +  macrophages by co-culture with endothelial cells. Moreover, CX 3 CL1 deficiency in human umbilical vein endothelial cells (HUVECs) attenuated the expression of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), whereas recombinant CX 3 CL1 treatment reversed this expression in co-cultured monocytes. Upon treatment with clodronate liposome, hepatic F4/80 high  macrophages were successfully depleted at day 2 and recovered similarly in CX 3 CR1 +/GFP  and CX 3 CR1 GFP/GFP  mice at week 4, suggesting a CX 3 CR1-independent replacement. However, F4/80 high  macrophages of CX 3 CR1 +/GFP  showed a stronger pro-inflammatory phenotype than CX 3 CR1 GFP/GFP  mice. In clodronate-treated chimeric CX 3 CR1 +/GFP  and CX 3 CR1 GFP/GFP  mice, CX 3 CR1 + F4/80 high  macrophages showed higher expression of IL-1β and TNF-α than CX 3 CR1 − F4/80 high  macrophages. In alcoholic liver injury, despite the similar frequency of hepatic F4/80 high  macrophages, CX 3 CR1 GFP/GFP  mice showed reduced liver injury, hepatic fat accumulation, and inflammatory responses than CX 3 CR1 +/GFP  mice. Thus, CX 3 CR1 could be a novel therapeutic target for pro-inflammatory macrophage-mediated liver injury.

CX3CR1 differentiates F4/80low monocytes into pro-inflammatory F4/80high macrophages in the liver