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Article Open Access

Intranasal instillation of miR‑410 targeting IL‑4/IL‑13 attenuates airway inflammation in OVA‑induced asthmatic mice

  • Authors:
    • Rong Jin
    • Sujuan Hu
    • Xiaomei Liu
    • Renzheng Guan
    • Ling Lu
    • Rongjun Lin
  • View Affiliations / Copyright

    Affiliations: Department of Pediatrics, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266000, P.R. China
    Copyright: © Jin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 895-900
    |
    Published online on: November 28, 2018
       https://doi.org/10.3892/mmr.2018.9703
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Abstract

Asthma is a common chronic inflammatory respiratory disease characterised by airway inflammation and hyperresponsiveness. The present study was designed to clarify the effect of intranasal miR‑410 administration in an ovalbumin (OVA)‑induced murine model of asthma. It was found that miR‑410 expression was significantly decreased in the lungs of OVA‑induced asthmatic mice (P<0.05) and miR‑410 was overexpressed via intranasal instillation. Bioinformatics indicated that the 3'‑untranslated regions of interleukin (IL)‑4 and IL‑13 messenger RNAs (mRNAs) contain miR‑410 binding sites. The IL‑4 and IL‑13 genes were confirmed to be miR‑410‑regulated using the dual‑luciferase reporter assay. Additionally, intranasal administration of miR‑410 markedly attenuated airway inflammation and reduced infiltration of inflammatory cells into bronchoalveolar lavage fluid (P<0.05) as determined by bronchoalveolar lavage fluid analysis. Moreover, miR‑410 significantly decreased the lung expression of IL‑4 and IL‑13 (P<0.05), although the levels of mRNAs encoding IL‑4 and IL‑13 in lungs did not change significantly as determined by real‑time PCR analysis. In conclusion, we found that intranasal administration of miR‑410 effectively inhibited airway inflammation in OVA‑induced asthmatic mice by targeting IL‑4 and IL‑13 at the post‑transcriptional level. miR‑410 is thus a promising treatment for allergic asthma.
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Copy and paste a formatted citation
Spandidos Publications style
Jin R, Hu S, Liu X, Guan R, Lu L and Lin R: Intranasal instillation of miR‑410 targeting IL‑4/IL‑13 attenuates airway inflammation in OVA‑induced asthmatic mice. Mol Med Rep 19: 895-900, 2019.
APA
Jin, R., Hu, S., Liu, X., Guan, R., Lu, L., & Lin, R. (2019). Intranasal instillation of miR‑410 targeting IL‑4/IL‑13 attenuates airway inflammation in OVA‑induced asthmatic mice. Molecular Medicine Reports, 19, 895-900. https://doi.org/10.3892/mmr.2018.9703
MLA
Jin, R., Hu, S., Liu, X., Guan, R., Lu, L., Lin, R."Intranasal instillation of miR‑410 targeting IL‑4/IL‑13 attenuates airway inflammation in OVA‑induced asthmatic mice". Molecular Medicine Reports 19.2 (2019): 895-900.
Chicago
Jin, R., Hu, S., Liu, X., Guan, R., Lu, L., Lin, R."Intranasal instillation of miR‑410 targeting IL‑4/IL‑13 attenuates airway inflammation in OVA‑induced asthmatic mice". Molecular Medicine Reports 19, no. 2 (2019): 895-900. https://doi.org/10.3892/mmr.2018.9703
Copy and paste a formatted citation
x
Spandidos Publications style
Jin R, Hu S, Liu X, Guan R, Lu L and Lin R: Intranasal instillation of miR‑410 targeting IL‑4/IL‑13 attenuates airway inflammation in OVA‑induced asthmatic mice. Mol Med Rep 19: 895-900, 2019.
APA
Jin, R., Hu, S., Liu, X., Guan, R., Lu, L., & Lin, R. (2019). Intranasal instillation of miR‑410 targeting IL‑4/IL‑13 attenuates airway inflammation in OVA‑induced asthmatic mice. Molecular Medicine Reports, 19, 895-900. https://doi.org/10.3892/mmr.2018.9703
MLA
Jin, R., Hu, S., Liu, X., Guan, R., Lu, L., Lin, R."Intranasal instillation of miR‑410 targeting IL‑4/IL‑13 attenuates airway inflammation in OVA‑induced asthmatic mice". Molecular Medicine Reports 19.2 (2019): 895-900.
Chicago
Jin, R., Hu, S., Liu, X., Guan, R., Lu, L., Lin, R."Intranasal instillation of miR‑410 targeting IL‑4/IL‑13 attenuates airway inflammation in OVA‑induced asthmatic mice". Molecular Medicine Reports 19, no. 2 (2019): 895-900. https://doi.org/10.3892/mmr.2018.9703
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