(A) Expression of Gpr84 in the liver after HFD feeding for 5 weeks (n = 7 tissues per group). Data are represented as relative to the gene expression in before HFD-fed mice. (B) Gpr84 expression in BM-derived monocytes, hepatic macrophages, Kupffer cells, hepatic stellate cells, and hepatocytes isolated from WT mice fed NC for 12 weeks (n = 5–6 per group). Data are represented as relative to the gene expression in macrophage. (C) Change of Gpr84 expression after HFD feeding (NC- vs. HFD-fed group, n = 5–6 per group). Data are represented as relative to the gene expression in NC-fed mice. (D) Flow cytometric analysis of BM-derived hepatic macrophage population and Tnf expression in WT and Gpr84^–/– mice fed the HFD for 12 weeks (n = 4 per group). BM-derived hepatic macrophages, CD45⁺Ly6C⁺F4/80⁺CD11b^hiCX3CR1⁺. (E) Flow cytometric analysis showing hepatic cell profile in BM-chimeric mice fed the HFD for 8 weeks (n = 8–9 per group) and NAS (n = 4 per group). WT recipient mice (CD45.1) after BM transplantation from WT or Gpr84^–/– donor mice (CD45.2). (F) Antiinflammatory effect of MCFA-stimulated GPR84 (n = 8 per group; independent experiments). Data are represented as relative to the gene expression in untreated cells. (G) Intracellular MCFA production in AML12 cells (mouse hepatocyte cell line) treated with palmitic acid for 48 hours (n = 8 per group; independent experiments). (H) Tnf expression in RAW264.7 cells cocultured with AML12 prestimulated by palmitic acid (C16:0; n = 6 per group; independent experiments). *P < 0.05; **P < 0.01 (Mann-Whitney U test: A and C–E upper, G; Student’s t test: E lower; and Kruskal-Wallis with Dunn’s post hoc test: F and H). All data are presented as the mean ± SEM.