Crystalline silica (cSiO2) is a mineral found in rocks; workers from the construction or denim industries are particularly exposed to cSiO2 through inhalation. cSiO2 inhalation increases the risk of silicosis and systemic autoimmune diseases. Inhaled cSiO2 microparticles can reach the alveoli where they induce inflammation, cell death, auto-immunity and fibrosis but the specific molecular pathways involved in these cSiO2 effects remain unclear. This systematic review aims to provide a comprehensive state of the art on omic approaches and exposure models used to study the effects of inhaled cSiO2 in mice and rats and to highlight key results from omic data in rodents also validated in human. The protocol of systematic review follows PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. Eligible articles were identified in PubMed, Embase and Web of Science. The search strategy included original articles published after 1990 and written in English which included mouse or rat models exposed to cSiO2 and utilized omic approaches to identify pathways modulated by cSiO2. Data were extracted and quality assessment was based on the SYRCLE’s Risk of Bias tool for animal studies. Rats and male rodents were the more used models while female rodents and autoimmune prone models were less studied. Exposure of animals were both acute and chronic and the timing of outcome measurement through omics approaches were homogeneously distributed. Transcriptomic techniques were more commonly performed while proteomic, metabolomic and single-cell omic methods were less utilized. Immunity and inflammation were the main domains modified by cSiO2 exposure in lungs of mice and rats. Less than 20% of the results obtained in rodents were finally verified in humans. Omic technics offer new insights on the effects of cSiO2 exposure in mice and rats although the majority of data still need to be validated in humans. Autoimmune prone model should be better characterised and systemic effects of cSiO2 need to be further studied to better understand cSiO2-induced autoimmunity. Single-cell omics should be performed to inform on pathological processes induced by cSiO2 exposure.

中文翻译：

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暴露于吸入结晶二氧化硅的大鼠或小鼠模型的组学方法的结果：系统评价

结晶二氧化硅 (cSiO2) 是一种存在于岩石中的矿物；建筑业或牛仔布行业的工人特别容易通过吸入接触 cSiO2。吸入 cSiO2 会增加患硅肺病和全身性自身免疫性疾病的风险。吸入的 cSiO2 微粒可以到达肺泡，引起炎症、细胞死亡、自身免疫和纤维化，但参与这些 cSiO2 效应的具体分子途径仍不清楚。本系统综述旨在提供有关组学方法和暴露模型的全面最新技术，用于研究吸入 cSiO2 对小鼠和大鼠的影响，并强调在啮齿类动物中也得到验证的组学数据的关键结果。系统评价的方案遵循 PRISMA（系统评价和荟萃分析的首选报告项目）指南。合格的文章在 PubMed、Embase 和 Web of Science 中被确定。搜索策略包括 1990 年后发表的英文原创文章，其中包括暴露于 cSiO2 的小鼠或大鼠模型，并利用组学方法来识别 cSiO2 调节的途径。数据提取和质量评估基于用于动物研究的 SYRCLE 偏差风险工具。大鼠和雄性啮齿动物是使用较多的模型，而雌性啮齿动物和自身免疫倾向模型的研究较少。动物的暴露有急性和慢性两种，通过组学方法测量结果的时间分布均匀。转录组学技术更常用，而蛋白质组学、代谢组学和单细胞组学方法则较少使用。免疫和炎症是小鼠和大鼠肺部 cSiO2 暴露改变的主要领域。在啮齿动物身上获得的结果只有不到 20% 最终在人类身上得到了验证。Omic 技术为小鼠和大鼠暴露于 cSiO2 的影响提供了新的见解，尽管大多数数据仍需要在人体中进行验证。应该更好地表征自身免疫倾向模型，并且需要进一步研究 cSiO2 的系统效应，以更好地了解 cSiO2 诱导的自身免疫。应进行单细胞组学来了解 cSiO2 暴露引起的病理过程。