This study was designed to investigate the effect of particulate matter with a diameter of ≤2.5 μm (PM2.5) on bleomycin (BLM) induced pulmonary fibrosis. Thirty-two Sprague Dawley rats were assigned into four groups (intratracheal instillation of 500 μL of PBS (control), 2 mg/kg PM2.5, 3.5 mg/kg BLM A5, and BLM plus 2.0 mg/kg PM2.5) and were fed for 14 days. All rats were sacrificed after the study. Lung tissues and bronchoalveolar lavage fluid were prepared for histological and biological analysis. We found that PM2.5 caused dose-trend pulmonary alveolitis and fibrosis. Histological scores, expression of α-SMA and Collagen I as well as contents of TNF-α and IL-6 in lung tissues were upregulated by treatment of PM2.5. PM2.5 did not change the percentage of neutrophils and macrophages. The expression of endoplasmic reticulum (ER) stress markers Chop and GRP78 was upregulated by treatment of PM2.5. In comparison with either PM2.5 or BLM treatment, BLM plus PM2.5 treatment induced higher histological scores, higher expression of α-SMA, collagen I, TNF-α, IL-6, Chop, and GRP78, with increased neutrophil counts and decreased macrophage counts. We concluded that PM2.5 instillation caused pulmonary alveolitis and fibrosis by stimulating ER stress responses in rat. PM2.5 also showed a synergistic effect on BLM-induced pulmonary fibrosis.

中文翻译：

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直径≤2.5μm的微粒物质通过刺激大鼠内质网应激来诱导和增强博来霉素诱导的肺纤维化。

本研究旨在调查直径≤2.5μm（PM2.5）的颗粒物对博来霉素（BLM）诱导的肺纤维化的影响。将32只Sprague Dawley大鼠分为四组（气管内滴入500μLPBS（对照），2 mg / kg PM2.5、3.5 mg / kg BLM A5和BLM加2.0 mg / kg PM2.5）。被喂了14天。研究后将所有大鼠处死。准备肺组织和支气管肺泡灌洗液用于组织学和生物学分析。我们发现PM2.5引起剂量趋势性肺泡炎和纤维化。PM2.5处理可上调肺组织的组织学评分，α-SMA和胶原I的表达以及TNF-α和IL-6的含量。PM2.5不会改变中性粒细胞和巨噬细胞的百分比。内质网（ER）应激标志物Chop和GRP78的表达上调PM2.5。与PM2.5或BLM治疗相比，BLM加PM2.5治疗可诱导更高的组织学评分，更高的α-SMA，胶原I，TNF-α，IL-6，Cop和GRP78表达，中性粒细胞计数和巨噬细胞数量减少。我们得出的结论是，通过刺激大鼠内质网应激反应，滴入PM2.5会引起肺泡炎和纤维化。PM2.5还显示出对BLM诱导的肺纤维化的协同作用。我们得出的结论是，通过刺激大鼠内质网应激反应，滴入PM2.5会引起肺泡炎和纤维化。PM2.5还显示出对BLM诱导的肺纤维化的协同作用。我们得出的结论是，滴注PM2.5可通过刺激大鼠ER应激反应而引起肺泡炎和纤维化。PM2.5还显示出对BLM诱导的肺纤维化的协同作用。