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Fig. 2 | Particle and Fibre Toxicology

Fig. 2

From: Diesel Exhaust Particle (DEP)-induced glucose intolerance is driven by an intestinal innate immune response and NLRP3 activation in mice

Fig. 2

DEP-induced gut inflammation and glucose intolerance do not depend on adaptive immunity. Oral exposure of Rag2-/- mice to diesel exhaust particles (DEP) or PBS for 4 months. A Absolute numbers and frequencies of CCR2+ pro-inflammatory and CCR2− anti-inflammatory/resident colon macrophages. B Glucose tolerance tests (GTT), insulin and body weight. C Insulinogenic index (ratio of AUC insulin and glucose). D Cholesterol, high-density lipoproteins (HDL), and triglycerides (TG). E Plasma TNF and IL-6. F Liver enzymes alkaline phosphatase (AP) and alanine transaminase (ALAT). G Frequencies of adipose tissue macrophages (ATM; F4/80+ among CD45+) and subpopulations DN: double negative. Data are shown as mean±SEM of pooled data from two independent experiments, with each data point representing an individual mouse. GTT and insulin values were compared by two-way ANOVA, all other parameters by a two-tailed, unpaired Mann-Whitney U test with two tailed distribution (*p < 0.05, **p < 0.01, ***p < 0.001). DEP: Diesel exhaust particles, PBS: Phosphate-buffered saline

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