PM2.5通过NF-κB/NLRP3途径促进金黄色葡萄球菌肺炎的研究
Staphylococcus aureus Pneumonia Aggravation by PM2.5 via NF-κB/NLRP3 Pathway
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摘要: 细颗粒物(PM2.5)引发的呼吸系统疾病近年来成为公众关注焦点。为探究PM2.5在金黄色葡萄球菌肺炎中产生的效应及其相关分子机制，将Balb/c小鼠随机分成6组：A.生理盐水对照，B.5 mg·kg-1 PM2.5，C.肺炎模型，D.肺炎模型+0.05 mg·kg-1 PM2.5，E.肺炎模型+0.5 mg·kg-1 PM2.5，F.肺炎模型+5 mg·kg-1 PM2.5，进行为期7 d的PM2.5气道滴注暴露后，用细菌滴鼻构建金黄色葡萄球菌肺炎模型。结果发现，PM2.5暴露造成了小鼠肺部损伤并促进了金黄色葡萄球菌肺炎，并随着PM2.5浓度的升高愈发显著，体现为小鼠肺部出现了更显著的气道重塑、炎症细胞浸润现象，肺纤维化程度加深。其分子机制是PM2.5首先引发小鼠肺部产生氧化应激，促进核因子κB (NF-κB)信号通路的激活，进而介导炎症小体NLRP3的活化，导致白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)表达升高，最终恶化了金黄色葡萄球菌肺炎。Abstract: PM2.5-induced respiratory diseases have become a public concern in recent years. To investigate the effect of PM2.5 on Staphylococcus aureus pneumonia and its related molecular mechanisms, Balb/c mice were randomly divided into 6 groups: A. saline control; B. 5 mg·kg-1 PM2.5; C. pneumonia model; D. pneumonia model+0.05 mg·kg-1 PM2.5; E. pneumonia model+0.5 mg·kg-1 PM2.5; F. pneumonia model+5 mg·kg-1 PM2.5. One-week instillation of PM2.5 was carried out, following by bacterial nasal inhalation to construct the Staphylococcus aureus pneumonia model. Results showed that PM2.5 exposure caused lung injury in mice and aggravated the symptom of Staphylococcus aureus pneumonia, which became more severe with the increase of PM2.5 concentration. It was observed that more significant airway remodeling and inflammatory cell infiltration occurred in mice lung, and the degree of pulmonary fibrosis was deepened. The proposed molecular mechanism was that PM2.5 first induced oxidative stress in mice lung, promoted the activation of NF-κB signaling pathway, and then mediated the activation of NLRP3, leading to an increased expression of inflammatory cytokines IL-1β and TNF-α. As a result, Staphylococcus aureus pneumonia could be aggravated by PM2.5.
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Key words:
- PM2.5 /
- Staphylococcus aureus pneumonia /
- mice /
- oxidative stress /
- NF-κB /
- NLRP3
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