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The absence of the IL-1R-dependent Th17 response in NO2-promoted allergic airway disease correlates with exacerbation of AHR.

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posted on 19.09.2013 by Rebecca A. Martin, Jennifer L. Ather, Rebecca Daggett, Laura Hoyt, John F. Alcorn, Benjamin T. Suratt, Daniel J. Weiss, Lennart K. A. Lundblad, Matthew E. Poynter

C57BL/6 (WT), IL-1R-/-, and STAT6-/- mice were subjected to NO2-promoted allergic sensitization, challenged, and analyzed 48 hours following the final antigen challenge. BAL total cells were quantified (A) and Macs (B), PMNs (C), and Eos (D) were calculated based on cell fractions. Methacholine responsiveness was performed by invasive forced oscillation technique. The percent baseline and average percent baseline per dose of methacholine were calculated for R (E-F) and E (G-H), as determined by the single-compartment model [47]. Quantitative RT-PCR was performed to measure gene expression for Cxcl5 (I), Lcn2 (J), Gob5 (K), and Muc5ac (L). Th2 cytokines IL-4 (M), IL-5 (N), and IL-13 (O), the Th1 cytokine IFNγ (P), and the Th17 cytokines IL-17A (Q), IL-17F (R), IL-22 (S), and IL-21 (T) were quantified by Milliplex. The dashed line in M, S, and T signifies the lower limit of detection in the assay. Statistics were performed by 1-way ANOVA (A-D and I-T) or 2-way ANOVA (F and G) and Tukey post-hoc analysis. **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05 compared to non-inflamed unless otherwise indicated by brackets. n = 5-8/group.