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.
摘要：
先前的研究报道了肠道微生物群失调与哮喘发生之间的相关性。本研究旨在探讨益生菌鼠李糖乳杆菌76(LR76)对卵清蛋白(OVA)过敏小鼠哮喘的影响及LR76对哮喘粘液分泌的影响机制。OVA过敏小鼠补充LR76,用LR76上清液(LR76-s)处理白细胞介素-13(IL-13)诱导的16HBE细胞,观察LR76的作用。在OVA致敏小鼠中，LR76减轻了肺组织中的炎性细胞浸润并减少了BALF的炎性细胞计数。mRNA的表达水平，包括Il4、Il5、Il13、Il25、Tgfb1、Il10和Ifng，与OVA组相比，LR76组小鼠的肺组织中降低。MUC5AC表达下调，而补充LR76后，OVA过敏小鼠的肺组织中SCGB1A1上调，与LR76-s孵育后，IL-13诱导的16HBE细胞中SCGB1A1上调。LR76和LR76-s下调蛋白质的表达，包括STAT6、p-STAT6和SPDEF，STAT6和SPDEF的mRNA。总之,LR76通过下调STAT6/SPDEF途径减轻OVA过敏小鼠的气道炎症和Th2反应，并改善哮喘模型中小鼠肺组织和16HBE细胞的粘液分泌。
