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Sulfur dioxide-enhanced asthma susceptibility is involved with inhibition of bitter taste transduction in mouse lung
Environmental Toxicology and Pharmacology ( IF 4.3 ) Pub Date : 2022-07-28 , DOI: 10.1016/j.etap.2022.103938
XiuJuan Li 1 , HuiLan Yi 2
Affiliation  

Sulfur dioxide (SO2) may induce asthma-like symptoms or worsen existing asthma, but the underlying mechanism is still unclear. In this study, the relationship between SO2 exposure, asthma development, and bitter taste transduction was analyzed using ovalbumin (OVA)-induced and SO2-aggravated asthma models. The results showed that twenty-seven and twelve bitter taste receptors (Tas2rs) were detectable in mouse trachea and lung, respectively, and that all of them were nearly down-regulated in OVA-induced BALB/c and C57BL/6 asthmatic mice. SO2 exposure alone did not trigger a distinct asthma-like phenotype, but the combination of SO2 and OVA allergen caused more severe asthma symptoms in mice including enhanced inflammatory cells infiltration, thickened airway walls, increased mucus secretion, and elevated expression of proinflammatory and Th2 cytokines (TNF-α, IL-4, IL-5, IL-13). Furthermore, SO2 enhanced the transcriptional repression of Tas2rs in OVA-induced asthmatic mice. These results indicated that the occurrence of mice asthma was correlated with the inhibition of bitter taste transduction, and more severe airway inflammation and injury were accompanied with an enhanced inhibition of bitter taste transduction. Our findings suggest that SO2 inhalation may amplify Th2 inflammatory responses in the lung of asthmatic mice by inhibiting bitter taste transduction, and thereby exacerbate asthma symptoms.



中文翻译:

二氧化硫增强哮喘易感性与抑制小鼠肺中苦味转导有关

二氧化硫 (SO 2 ) 可能会诱发哮喘样症状或加重现有哮喘,但其潜在机制仍不清楚。在这项研究中,使用卵白蛋白 (OVA) 诱导和 SO 2加重的哮喘模型分析了 SO 2暴露、哮喘发展和苦味转导之间的关系。结果表明,在小鼠气管和肺中分别检测到27个和12个苦味受体(Tas2rs),并且在OVA诱导的BALB/c和C57BL/6哮喘小鼠中几乎全部下调。单独的SO 2暴露不会引发明显的哮喘样表型,但 SO 2的组合和 OVA 过敏原在小鼠中引起更严重的哮喘症状,包括炎症细胞浸润增强、气道壁增厚、粘液分泌增加以及促炎和 Th2 细胞因子(TNF-α、IL-4、IL-5、IL-13)表达升高。此外,SO 2增强了OVA 诱导的哮喘小鼠中Tas2rs的转录抑制。这些结果表明,小鼠哮喘的发生与苦味传导的抑制有关,更严重的气道炎症和损伤伴随着苦味传导的抑制增强。我们的研究结果表明 SO 2吸入可通过抑制苦味转导放大哮喘小鼠肺部的Th2炎症反应,从而加剧哮喘症状。

更新日期:2022-07-28
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