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. 2014 Aug 25;111(36):13145–13150. doi: 10.1073/pnas.1412008111

Fig. 5.

Fig. 5.

Clostridia-induced IL-22 regulates allergen access to the bloodstream. (A) Expression of Il22 in LPL from neonatal Abx-treated mice without Clostridia colonization, or at 6 d after weaning and colonization. (B) Serum Ara h 6 at indicated time points after PN gavage in NT or Abx mice treated with or without one i.p. injection of IL-22-Fc, or by Clostridia colonization. (C) Serum Ara h 6 at indicated time points after PN gavage in Abx-treated Clostridia-colonized mice injected i.p. with neutralizing antibody to IL-22 or an isotype control. All mice in B and C received PN at 6 d after weaning, and serum levels of Ara h 6 were measured by capture ELISA (n = 5–10 mice per group, pooled from at least two experiments). (D) Expression of Reg3b in whole-tissue extracts from Abx-treated Clostridia-colonized mice treated with neutralizing antibody to IL-22 or an isotype control and sensitized with PN/CT (n = 11 mice per group, pooled from four experiments). (E) Concentration of IL-4 in culture supernatants from splenocytes of mice from D (n = 7 mice per group, representative of two experiments). (F) Concentration of PN-specific and total IgE in serum collected 24 h after challenge for mice in D (n = 11 mice per group, pooled from four experiments). (G) Concentration of IL-17 in culture supernatants from splenocytes from mice in D (n = 7 mice per group, representative of two experiments). (H) Concentration of PN-specific IgG in serum collected 24 h after challenge for mice in D (n = 11 mice per group, pooled from four experiments). (I) UniFrac analysis of fecal microbiota throughout the sensitization protocol (n = 4 mice per group). *P < 0.05, **P < 0.01 ***P < 0.001 by two-way ANOVA with Bonferroni posttest (A, B, and D) or Student t test (C and G).