Lactobacillus rhamnosus 76 alleviates airway inflammation in ovalbumin-allergic mice and improves mucus secretion by down-regulating STAT6/SPDEF pathway

鼠李糖乳杆菌76通过下调STAT6/SPDEF通路减轻卵清蛋白过敏小鼠的呼吸道炎症并改善粘液分泌

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作者:Yangfan Hou, Shuping Zheng, Fan Zou, Dan Wang, Hongju Da, Yong Zhou, Xinping Fan, Jianghao Liu, Hongyan Zhao, Jin He, Hongxin Li, Xiuzhen Sun, Yun Liu

Abstract

Previous studies have reported a correlation between the dysregulation of intestinal microbiota and the occurrence of asthma. This study aimed to investigate the effect of probiotic Lactobacillus rhamnosus 76 (LR76) on ovalbumin (OVA)-allergic mice and the mechanism of LR76 affecting mucus secretion in asthma. OVA-allergic mice were supplemented with LR76, and 16HBE cells induced by interleukin-13 (IL-13) were treated with LR76 supernatant (LR76-s) to observe the effect of LR76. In OVA-sensitized mice, LR76 alleviated the inflammatory cell infiltration in lung tissue and reduced the inflammatory cell counts of BALF. The expression level of mRNA, including Il4, Il5, Il13, Il25, Tgfb1, Il10, and Ifng, was decreased in the lung tissue of mice in the LR76 group compared with the OVA group. MUC5AC expression was down-regulated, while SCGB1A1 was up-regulated in the lung tissue of OVA-allergic mice after being supplemented with LR76 and in 16HBE cells induced by IL-13 after incubating with LR76-s. LR76 and LR76-s down-regulated the expression of proteins, including STAT6, p-STAT6, and SPDEF, and mRNA of STAT6 and SPDEF. In conclusion, LR76 alleviated airway inflammation and Th2 response in OVA-allergic mice and improved the mucus secretion of mouse lung tissue and 16HBE cells in the asthma model by down-regulating STAT6/SPDEF pathway.

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