背景:过敏性哮喘被认为是由2型免疫介导的炎症性疾病。尽管药物开发取得了实质性进展,但进行性哮喘的治疗仍不能令人满意。香菇多糖(LTN),一种来自香菇的特定多糖,具有抗炎和免疫调节功能。然而,香菇多糖对哮喘的作用和潜在机制尚不清楚.
目的:本研究探讨香菇多糖对HDM(屋尘螨)诱导的哮喘中过敏性气道炎症和上皮屏障功能障碍的调节作用。
方法:HDM诱导的C57BL/6小鼠腹腔注射不同剂量的香菇多糖,观察香菇多糖对哮喘变应性气道炎症和上皮屏障功能障碍的影响。
方法:小鼠于第0、1、2天和第8至12天鼻内给药HDM提取液,建立过敏性哮喘模型。在第8至12天,小鼠在HDM攻击前1小时腹膜内施用不同剂量的香菇多糖(5/10/20mg/kg)。在第14天,收获样品用于分析。细胞计数,流式细胞术,ELISA,HE和PAS染色,IF染色,西方印迹,RT-PCR,并进行了生物信息学分析,以探讨香菇多糖在哮喘中的潜在作用和机制。
结果:我们的研究表明,香菇多糖治疗可显着改善实验性小鼠的过敏性气道炎症和上皮屏障功能障碍。香菇多糖治疗后,嗜酸性粒细胞计数显著减少,伴随着2型细胞因子的减少。还观察到治疗后上皮屏障功能障碍的逆转。治疗机制涉及抑制PI3K/AKT/NF-κB途径。
结论:我们的研究揭示了香菇多糖在过敏性气道炎症和上皮屏障受损中的保护作用。提示LTN可能是哮喘治疗的创新和有希望的候选药物.
BACKGROUND: Allergic asthma has been regarded as an inflammatory disease mediated by type 2 immunity. The treatment of progressive forms of asthma remains unsatisfactory despite substantial progress in drug development.
Lentinan (LTN), a specific polysaccharide derived from Lentinus edodes, exhibits anti-inflammatory and immunomodulatory functions. Nevertheless, the effect and underlying mechanisms of
Lentinan on asthma remain unclear.
OBJECTIVE: This research investigated the regulatory role of Lentinan on allergic airway inflammation and epithelial barrier dysfunction in HDM (house dust mite)-induced asthma.
METHODS: HDM-induced C57BL/6 mice received different dosages of Lentinan through intraperitoneal injections, to observe the effect of
Lentinan against allergic airway inflammation and epithelial barrier dysfunction in asthma.
METHODS: Mice were intranasally administered HDM extract solution on days 0, 1, 2 and on days 8 to 12, establishing the allergic asthma model. On days 8 to 12, mice were intraperitoneally administered varying doses of
Lentinan (5/10/20mg/kg) 1h before HDM challenge. On day 14, samples were harvested for analysis. Cell counting, flow cytometry, ELISA, HE and PAS staining, IF staining, western blotting, RT-PCR, and bioinformatic analysis were conducted to delve into the underlying functions and mechanisms of Lentinan in asthma.
RESULTS: Our study revealed that the treatment of Lentinan significantly ameliorated allergic airway inflammation and improved epithelial barrier dysfunction in experimental mice. Following
Lentinan treatment, there was a significant reduction in eosinophil counts, accompanied by a diminished presence of type 2 cytokines. Reversal of epithelial barrier dysfunction after treatment was also observed. The therapeutic mechanism involved suppression of the PI3K/AKT/ NF-κB pathway.
CONCLUSIONS: Our research illuminated the protective role of Lentinan in allergic airway inflammation and impaired epithelial barrier, suggesting LTN could be an innovative and promising candidate for asthma treatment.