Fig. 6

NLRP3 inflammasome activation and IL-1β secretion contribute to DEP-induced gut inflammation and glucose intolerance. A Protein expression of IL-1β in supernatant of wild-type and Nlrp3-/- peritoneal macrophages exposed in vitro to 125 µg/mL diesel exhaust particles (DEP) or PBS in the presence or absence of MCC950 (Nlrp3-inhibitor). B Absolute numbers of total, CCR2⁺ pro-inflammatory and CCR2⁻ anti-inflammatory/resident colon macrophages and their frequencies in Nlrp3-/- mice exposed to diesel exhaust particles (DEP) or PBS for 6 months. C GTT, insulin, body weight and insulinogenic index. D-E Wild-type mice were treated with anti-IL-1β or control antibody (anti-cyclosporin A; CSA) after they developed impaired glucose tolerance. D Absolute numbers of total, CCR2⁺ pro-inflammatory and CCR2⁻ anti-inflammatory/resident colon macrophages. E GTT, insulin, body weight and insulinogenic index after two weeks of anti-IL-1β treatment. Data are shown as mean±SEM. B-E represent one experiment, A pooled data from two independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001, unpaired Mann-Whitney U test with two tailed distribution, two-way ANOVA was used to analyze insulin and glucose values. DEP: Diesel exhaust particles, LPS: Lipopolysaccharide, PBS: Phosphate-buffered saline