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Erschienen in: Inflammation Research 10/2015

01.10.2015 | Original Research Paper

Adenovirus-mediated interleukin-35 gene transfer suppresses allergic airway inflammation in a murine model of asthma

verfasst von: Yan Li, Xiuhe Pan, Xiao Peng, Shubo Li, Yanchun Zhou, Xiaoxuan Zheng, Mingcai Li

Erschienen in: Inflammation Research | Ausgabe 10/2015

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Abstract

Objective and design

Asthma is thought to result from the generation of T helper type 2 (Th2) responses, leading to bronchial inflammation. Interleukin (IL)-35 is a recently described member of IL-12 cytokine family that plays a critical role in influencing Th cell differentiation and inflammatory processes. The aim of this study was to examine the effect of adenovirus expressing IL-35 (AdIL-35) on allergic airway hyperresponsiveness (AHR) and inflammation in a mouse model of asthma.

Methods

BALB/c mice were subjected to an established model of allergic airway disease. AdIL-35 was administered intranasally and the effect of IL-35 on Th2 responses, pulmonary inflammation, goblet cell metaplasia, and AHR were assessed.

Results

Transfer of AdIL-35 significantly reduced the severity of AHR and numbers of inflammatory cells and levels of IL-4, IL-5, IL-13, and IL-17 in bronchoalveolar lavage fluid, compared with administration of a control virus. Moreover, AdIL-35 elevated the numbers of CD4+CD25+Foxp3+ regulatory T cells in the lungs. Histological analysis showed that AdIL-35 inhibited allergic lung tissue inflammation and mucus hypersecretion.

Conclusion

These results demonstrate that adenovirus-mediated delivery of interleukin-35 gene can mitigate allergic airway inflammation in experimental asthma and suggest that IL-35 may offer a novel therapeutic approach to treat allergic asthma.
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Metadaten
Titel
Adenovirus-mediated interleukin-35 gene transfer suppresses allergic airway inflammation in a murine model of asthma
verfasst von
Yan Li
Xiuhe Pan
Xiao Peng
Shubo Li
Yanchun Zhou
Xiaoxuan Zheng
Mingcai Li
Publikationsdatum
01.10.2015
Verlag
Springer Basel
Erschienen in
Inflammation Research / Ausgabe 10/2015
Print ISSN: 1023-3830
Elektronische ISSN: 1420-908X
DOI
https://doi.org/10.1007/s00011-015-0858-1

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