IL-27 alleviates airway remodeling in a mouse model of asthma via PI3K/Akt pathway.

Abstract

Purpose: Airway remodeling is one of the features of severe asthma. Previous study shows that IL-27 inhibits airway inflammation in asthmatic mice. However, the role of IL-27 on airway remodeling in OVA-induced asthmatic mice and its possible mechanism remain unclear. Methods: We established an ovalbumin (OVA)-induced asthmatic mice model. IL-27 were preventative administered to OVA-induced asthmatic mice. The total cells in Bronchoalveolar lavage fluid (BALF) and Airway hyperresponsiveness (AHR) were measured. The lung tissues were performed by Hematoxylin and eosin (HE) staining to estimate the pathological changes. Masson staining was used to observe the collagen deposition area. The expression of α-smooth muscle actin (α-SMA) and Type I collagen was measured by immunohistochemistry, western blot, and quantitative reverse transcription polymerase chain reaction (qRT-PCR). Additionally, western blot was also used to measure the expression of phosphorylated-Akt (p-Akt) in each group. Results: IL-27 group showed significant inhibitory effect on the α-SMA and Type I collagen. The expression of p-Akt in the tissues of asthma model was increased and inhibited by IL-27. Conclusions: IL-27 can alleviate airway remodeling in OVA-induced asthmatic mice, and the mechanism may relate to PI3K/Akt pathway.

• Authors: Xin Li, Ling Zhou, Zewen Zhang, Yuanyuan Liu, Ju Liu, Caiqing Zhang
• Journal: Experimental lung research (Exp Lung Res) 2020 Apr - May Vol. 46 Issue 3-4 Pg. 98-108 ISSN: 1521-0499 [Electronic] England
• PMID: 32164467 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Interleukin-27
• Proto-Oncogene Proteins c-akt

Topics

• Airway Remodeling (drug effects)
• Animals
• Asthma (drug therapy, metabolism)
• Drug Evaluation, Preclinical
• Female
• Interleukin-27 (pharmacology, therapeutic use)
• Lung (drug effects, metabolism)
• Mice, Inbred BALB C
• Phosphatidylinositol 3-Kinases (metabolism)
• Proto-Oncogene Proteins c-akt (metabolism)