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Enhanced osteopontin expression in a murine model of allergen-induced airway remodelling.

机译：在变应原诱导的气道重塑小鼠模型中增强骨桥蛋白的表达。

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BACKGROUND: Airway remodelling is a central pathophysiological feature of chronic asthma. A wide variety of cytokines and growth factors are likely to be involved in the development of airway remodelling. Osteopontin (OPN) is a cytokine with pro-fibrotic properties; however, its role in airway remodelling in asthma has not been explored. OBJECTIVE: To determine the expression and cellular sources of OPN in a murine model of chronic allergen-induced airway remodelling. METHODS: BALB/c mice were sensitized and exposed to ovalbumin (OVA) or saline inhalations for 5 weeks and killed 24 h after the last inhalation. The following parameters of inflammation and remodelling were assessed: differential cell counts in bronchoalveolar lavage (BAL) fluid lung collagen content (colorimetric biochemical assay) and peribronchial smooth muscle content (immunohistochemistry, followed by image analysis). OPN expression in BAL and lung tissue was determined by PCR and ELISA. The cellular source and distribution of OPN were evaluated by immunohistochemistry and immunofluorescence. RESULTS: OPN expression is up-regulated in lung tissue and in BAL fluid of OVA-treated mice and correlates with collagen content and peribronchial smooth muscle area. In addition, OPN significantly increases collagen deposition in vitro in a murine lung cell line. Cells producing OPN include the airway epithelium and cells of the submucosal inflammatory infiltrate (T cells, eosinophils, and macrophages). Positive staining for OPN was also observed in bronchial tissue from human asthmatic subjects. CONCLUSION: OPN expression in the lungs is increased in a murine model of allergen-induced chronic airway remodelling, suggesting a role for this cytokine in airway remodelling in asthma.
机译：背景：气道重塑是慢性哮喘的主要病理生理特征。气道重塑的发展可能涉及多种细胞因子和生长因子。骨桥蛋白（OPN）是一种具有促纤维化特性的细胞因子。然而，尚未探讨其在哮喘气道重塑中的作用。目的：确定OPN在慢性变应原诱导的气道重塑小鼠模型中的表达和细胞来源。方法：将BALB / c小鼠致敏并暴露于卵清蛋白（OVA）或盐水中吸入5周，并在最后一次吸入后24 h处死。评估了以下炎症和重塑参数：支气管肺泡灌洗（BAL）液中肺胶原含量（比色生化测定）和支气管周围平滑肌含量（免疫组织化学，然后图像分析）中的细胞计数差异。通过PCR和ELISA测定BAL和肺组织中的OPN表达。通过免疫组织化学和免疫荧光评价OPN的细胞来源和分布。结果：OVA处理小鼠的肺组织和BAL液中OPN表达上调，并与胶原含量和支气管周平滑肌面积相关。另外，OPN在鼠肺细胞系中体外显着增加胶原蛋白的沉积。产生OPN的细胞包括气道上皮和粘膜下炎性浸润的细胞（T细胞，嗜酸性粒细胞和巨噬细胞）。在人哮喘受试者的支气管组织中也观察到OPN阳性染色。结论：在变应原引起的慢性气道重塑的小鼠模型中，肺中OPN的表达增加，提示该细胞因子在哮喘气道重塑中的作用。

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