A mechanistic review-regulation of silica-induced pulmonary inflammation by IL-10 and exacerbation by Type I IFN.

IF 2 4区 医学 Q4 TOXICOLOGY
Inhalation Toxicology Pub Date : 2025-02-01 Epub Date: 2025-02-16 DOI:10.1080/08958378.2025.2465378
Hajime Kawasaki
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引用次数: 0

Abstract

Occupational exposure to crystalline silica (CS) is known to induce silicosis, a chronic lung disease characterized by the formation of granulomas and severe lung fibrosis. Specifically, individuals exposed to low doses of CS may develop silicosis after a decade or more of exposure. Similarly, in rat silicosis models exposed to occupationally relevant doses of α-quartz, there is an initial phase characterized by minimal and well-controlled pulmonary inflammation, followed by the development of robust and persistent inflammation. During the initial phase, the inflammation provoked by α-quartz is subdued by two mechanisms. Firstly, α-quartz particles are engulfed by alveolar macrophages (AMs) of the alternatively activated (M2) subtype and interstitial macrophages (IMs), limiting their interaction with other lung cells. Secondly, the anti-inflammatory cytokine, interleukin (IL)-10, is constitutively expressed by these macrophages, further dampening the inflammatory response. In the later inflammatory phase, IL-10-dependent anti-inflammatory state is disrupted by Type I interferons (IFNs), leading to the production of pro-inflammatory cytokines in response to α-quartz, aided by lipopolysaccharides (LPS). This review delves into the complex pathways involving IL-10, LPS, and Type I IFNs in α-quartz-induced pulmonary inflammation, offering a detailed analysis of the underlying mechanisms and identifying areas for future research.

IL-10调节二氧化硅诱导的肺部炎症和I型IFN加重的机制综述。
众所周知,职业性暴露于结晶二氧化硅(CS)可诱发矽肺病,这是一种以肉芽肿形成和严重肺纤维化为特征的慢性肺部疾病。具体而言,暴露于低剂量CS的个体可能在暴露10年或更长时间后发生矽肺病。同样,在暴露于职业相关剂量α-石英的大鼠矽肺模型中,初始阶段的特征是轻微且控制良好的肺部炎症,随后发展为强烈且持续的炎症。在初始阶段,α-石英引起的炎症受到两种机制的抑制。首先,α-石英颗粒被替代活化(M2)亚型的肺泡巨噬细胞(AMs)和间质巨噬细胞(IMs)吞噬,限制了它们与其他肺细胞的相互作用。其次,抗炎细胞因子白细胞介素(IL)-10由这些巨噬细胞组成性表达,进一步抑制炎症反应。在炎症后期,il -10依赖的抗炎状态被I型干扰素(ifn)破坏,导致在脂多糖(LPS)的帮助下,α-石英反应产生促炎细胞因子。本综述深入研究了IL-10、LPS和I型ifn在α-石英诱导的肺部炎症中的复杂途径,提供了潜在机制的详细分析,并确定了未来研究的领域。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Inhalation Toxicology
Inhalation Toxicology 医学-毒理学
CiteScore
4.10
自引率
4.80%
发文量
38
审稿时长
6-12 weeks
期刊介绍: Inhalation Toxicology is a peer-reviewed publication providing a key forum for the latest accomplishments and advancements in concepts, approaches, and procedures presently being used to evaluate the health risk associated with airborne chemicals. The journal publishes original research, reviews, symposia, and workshop topics involving the respiratory system’s functions in health and disease, the pathogenesis and mechanism of injury, the extrapolation of animal data to humans, the effects of inhaled substances on extra-pulmonary systems, as well as reliable and innovative models for predicting human disease.
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