Fig. 4

Mice treated with the CSF1R-inhibitor PLX5622 are devoid of tissue resident macrophages and protected from DEP-induced gut inflammation and glucose intolerance. Wild-type were mice pharmacologically depleted of macrophages by a diet containing the CSF1R-inhibitor PLX5622 and exposed to diesel exhaust particles (DEP) or PBS for 10 months. A Representative flow cytometry plots of colon macrophages and their subsets and fold change of absolute numbers in mice treated with PLX5622 compared to untreated controls. B Absolute numbers of total, CCR2⁺ inflammatory and CCR2⁻ anti-inflammatory/resident colon macrophages and their frequencies. C GTT, insulin, body weight and insulinogenic index. D Cholesterol, high-density lipoproteins (HDL), and triglycerides (TG). E Plasma TNF and IL-6. F Flow cytometric analysis of liver macrophages of CD45⁺ cells. CD11b was used to distinguish infiltrating macrophages (CD11b^high) and Kupffer cells (CD11b^low). G Liver enzymes. H Frequencies of adipose tissue macrophages (ATM) among CD45⁺ cells, distribution of ATM subpopulations among ATM. Data are presented as mean±SEM pooled from two independent experiments with each data point representing an individual mouse. *p < 0.05, **p < 0.01, ***p < 0.001, unpaired Mann-Whitney U test with two tailed distribution. Insulin and glucose values were analyzed using two-way ANOVA. DEP: Diesel exhaust particles, PBS: Phosphate-buffered saline, PLX: PLX5622.