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. 2017 May 12;7:1848. doi: 10.1038/s41598-017-02085-5

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Intranasal administration of mCRAMP induced the exacerbation of OVA-induced airway hyperresponsiveness. (A) timeline protocol (Day 0 to Day 24) of OVA-induced allergic airway inflammation and intranasal mCRAMP administration. (B) increasing doses of inhaled methacholine-induced airway obstruction were presented as Penh (% increase over baseline), which was calculated by dividing the Penh value of different doses of methacholine by the Penh value of PBS baseline. (C) representative H&E and PAS staining of lung sections (x100 magnification). Black arrows denote bright purple-stained mucin-producing goblet cells. Scale bars = 100 µm. The concentrations of serum OVA-specific IgE (D) as well as IL-4 (E) and KC (F) in the lung homogenates were determined. *P < 0.05, **P < 0.01. Data are representative from 2 independent experiments showing essentially similar results. Mice (n = 5) were used within each group for different treatments.