Figure 5 | Scientific Reports

Figure 5

From: Lack of NLRP3-inflammasome leads to gut-liver axis derangement, gut dysbiosis and a worsened phenotype in a mouse model of NAFLD

Figure 5

Nlrp3−/−-HFHC-fed mice showed increased bacterial translocation and AMPs. HFHC induced bacterial translocation, expressed as turbidity of cultured mesenteric lymph nodes, that was further increased in Nlrp3−/−-HFHC-fed mice (a). Representative cropped Western blotting and densitometric analysis for caecal and ileal tight junction proteins (b-c) (full-length blots are presented in Supplementary Fig. S2). Regarding AMPs, in the caecum β-defensin 1 and 2 (BD1–2) expression was unchanged, whereas a lower expression of resistin-like molecule β (RELMβ) and angiogenin 4 (ANG4) has been observed after HFHC diet but independently from the genotype (d). In the ileum, HD4 and BD2 gene expression was not modified by neither diet or genotype, BD1 and RELMβ were reduced in HFHC-fed mice, whereas diet-induced reduction of ANG4 was more pronounced in NLRP3-deficient mice (e). Mean ± SE: *p < 0.05; **p < 0.01; ç p < 0.05 vs Wt-Chow diet; çç p < 0.01 vs Wt-Chow diet; ççç p < 0.001 vs Wt-Chow diet; #p < 0.05 vs Nlrp3−/−-Chow diet; ##p < 0.01 vs Nlrp3−/−-Chow diet; ###p < 0.001 vs Nlrp3−/−-Chow diet; ùù p < 0.01 vs Wt-HFHC.

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