Fig. 3

CCR2-/- mice with deficient monocyte recruitment are prevented from DEP-induced gut inflammation and glucose intolerance. CCR2-/- mice were orally exposed to diesel exhaust particles (DEP) or PBS for 8 months. A Representative flow cytometry plots of total colon macrophages and CCR2⁺ and CCR2⁻ macrophages. Fold change of total, Ly6C^high inflammatory and Ly6C^low anti-inflammatory/resident colon macrophages in CCR2-/- mice compared to wild-type mice. B Colon gene expression of immune cell markers in CCR2-/- mice exposed to DEP relative to PBS after 8 months of exposure. C Absolute numbers of total, Ly6C^high inflammatory and Ly6C⁻ anti-inflammatory/resident colon macrophages and their frequencies. D Glucose tolerance tests (GTT), insulin, body weight and insulinogenic index. E Plasma TNF and IL-6. F Cholesterol, high-density lipoproteins (HDL), and triglycerides (TG). G Liver enzymes and inflammatory gene expression in the liver. H Frequencies of macrophages in the adipose tissue (ATM) among CD45⁺ cells, relative distribution of ATM subpopulations, and inflammatory gene expression in adipose tissue of CCR2-/- mice exposed to DEP compared to control mice exposed to PBS. Data are presented as mean±SEM pooled from three experiments, with each data point representing an individual mouse. **p < 0.01, unpaired Mann-Whitney U test with two tailed distribution. Glucose and insulin measures were compared by two-way ANOVA. DEP: Diesel exhaust particles, PBS: Phosphate-buffered saline