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. 2019 Dec 12;10:2893. doi: 10.3389/fimmu.2019.02893

Figure 3.

Figure 3

Crosstalk between tissue-specific inflammation and macrophage function in NAFLD. Schematic overview of the crosstalk between various organs, their specific immune cells and inflammatory mediators during NAFLD. Obesity-associated low-grade, chronic inflammation and altered gut microbiome impacts immune cell crosstalk between the gut, circulating monocytes/macrophages, and the liver. In addition, obesity-associated adipocyte expansion promotes hypoxia leading to adipose tissue (AT) inflammation, activation of adipose tissue macropahes (ATMs) and fuels infiltration of various immune cells and inflammatory mediator production (e.g., FFAs, ROS, cytokines, chemokines) to be sensed by circulating macrophages and hepatocytes. Collectively these processes alter hepatocellular lipid metabolism, contributing to steatosis and proinflammatory cytokine (IL-17, TNF, IFNγ, IL-6) and chemokine production (CCL2, CXCL9, CXCL10). Moreover, this inflammatory state activates hepatic stellate cells (HSCs) and Kupffer cells (KCs) in turn contributing to extracellular matrix deposition (collagen fibers) and progression to fibrosis.