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. Author manuscript; available in PMC: 2012 Jun 27.
Published in final edited form as: Nat Med. 2007 Apr 15;13(5):570–578. doi: 10.1038/nm1580

Figure 2.

Figure 2

Opn-s blockade at priming reduces allergic disease. (a) Experimental protocol used to neutralize endogenous Opn-s during sensitization. BALB/c mice received two doses of anti-Opn or Ig control before each OVA/alum sensitization. (b) BAL differentials are expressed as mean ± s.e.m. n = 6–8 mice per group, three independent experiments. ***P = 0.0008, *P = 0.0209 (unpaired Student’s t-test). (c) AHR responses for enhanced pause (Penh) in mice treated with either anti-Opn or Ig. **P = 0.010 (two-way repeated-measures analysis of variance (ANOVA), and unpaired Student’s t-test). (d) Lung inflammation (top) and mucus secretion (bottom). *P = 0.0269, **P = 0.0156 (unpaired Student’s t-test). Scale bar, 100 μm. (e) Lung levels of IL-4 (**P = 0.0015), IL-13 (*P = 0.0255), IL-10 (**P = 0.007), IFN-γ (P = 0.068), IL-12 (**P = 0.0026) and CCL11 (*P = 0.0377). (f) Levels of IL-4 (***P < 0.0001), IL-13 (*P = 0.0121), IL-10 (***P = 0.0002) and IFN-γ (**P = 0.0014) in supernatants of OVA-stimulated DLNs. Serum levels of OVA-specific IgE (*P = 0.0328), IgG1 (**P = 0.0072) and IgG2a (*P = 0.0437). (g) BALB/c mice were sensitized as above and challenged with OVA on day 18. Anti-Opn or the Ig control were administered before each sensitization. Percentages of T1/ST2+ DLN cells gated on CD3+CD4+ T cells are shown, along with isotype control staining for the T1/ST2 marker. One representative experiment of three. n = 3–5 mice per group. Lung levels of CCL17 (P = 0.1749) and CCL22 (*P = 0.0115) are shown.