Fig. 2: Contribution of the gut microbiota to local and systemic inflammation in Zfp36−/− mice. | Mucosal Immunology

Fig. 2: Contribution of the gut microbiota to local and systemic inflammation in Zfp36−/− mice.

From: The RNA-binding protein tristetraprolin regulates RALDH2 expression by intestinal dendritic cells and controls local Treg homeostasis

Fig. 2

a–d Feces were collected from WT or Zfp36−/− mice at 5 months of age for bacterial DNA sequencing. a Total fecal bacteria levels by absolute quantitative RTqPCR (n = 4–10 mice/group). b Shannon and Simpson alpha-diversity indexes. c Principal coordinates analyses of the Morisita–Horn and Bray–Curtis beta-diversity metrics. In these analyses, genotype explains 13% and 23%, respectively, of the dataset variance (ANOSIM analyses, 1000 permutations, p < 0.05). d Families and genera significantly affected in Zfp36−/− mice (q value < 0.1). e Modulation of gut microbiota by broad-spectrum antibiotic therapy (ABT) in Zfp36−/− mice and WT controls, from 6 weeks of age until the day of sacrifice at 20 weeks of age, followed by flow cytometry, ELISA, and RTqPCR experiments. f Total fecal bacteria levels by absolute quantitative RTqPCR in feces collected 2 months after the start of ABT (n = 8–12 mice/group, pooled from two independent experiments). g Lipocalin-2 levels by ELISA in feces collected before (n = 11–13 mice/group, pooled from two independent experiments) and 2 months after the start of ABT (n = 5–7 mice/group). h Neutrophil infiltration of the small intestinal lamina propria (SI LP) and mesenteric lymph nodes (MLN) by flow cytometry (n = 12–17 mice/group, pooled from three independent experiments). i Cytokine and antimicrobial peptide gene expression in total ileum by RTqPCR, expressed in arbitrary units normalized against Actb mRNA levels and relative to the WT control group (n = 10-13 mice/group, pooled from two independent experiments). j Weight and k arthritis severity follow-up (n = 12–17 mice/group, pooled from three independent experiments). (l) Serum levels of lipocalin-2 by ELISA (n = 8–13, pooled from two independent experiments). m Neutrophil infiltration of the spleen (n = 12–17 mice/group, pooled from three independent experiments) and n the skin (n = 9–12 mice/group, pooled from two independent experiments) by flow cytometry. o IL-17 producing cells of the skin by flow cytometry (n = 12–15 mice/group, pooled from three independent experiments). Results are given as median ± interquartile range and each dot represents a single mouse. Statistical significance (ns nonsignificant, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001) was assessed by two-way ANOVA test (f–i, l–o).

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