纳米塑料在人类肠道和小鼠小胶质细胞中激活TLR4/p38介导的促炎反应。

IF 4.2 3区 环境科学与生态学 Q2 ENVIRONMENTAL SCIENCES
Joana Antunes , Paula Sobral , Marta Martins , Vasco Branco
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引用次数: 0

摘要

纳米塑料在环境中的新月形存在引发了人们对其对健康潜在影响的担忧。这项研究将人类结肠腺癌细胞(HT29)和小胶质细胞(N9)暴露于纳米塑料(25nm、50nm和100nm聚苯乙烯)中,以研究它们的炎症反应,这对身体防御至关重要。尽管细胞毒性通常保持较低,但HT29细胞表现出p50和p38表达的显著上调,伴随着TLR4表达的升高,而N9细胞则表现出这些蛋白不太明显的上调。此外,纳米塑料暴露增加了IL-1ß水平,部分通过预暴露于TLR4或p38抑制剂而减弱。有趣的是,暴露于纳米塑料的N9细胞iNOS mRNA显著增加。这种作用通过预先暴露于TLR4或p38抑制剂而被完全阻止,而TNF-αmRNA水平保持相对稳定。这些发现强调了纳米塑料激活炎症途径的潜力,其反应动力学因细胞类型而异。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Nanoplastics activate a TLR4/p38-mediated pro-inflammatory response in human intestinal and mouse microglia cells

Nanoplastics activate a TLR4/p38-mediated pro-inflammatory response in human intestinal and mouse microglia cells

The crescent presence of nanoplastics in the environment raises concerns regarding their potential impact on health. This study exposed human colon adenocarcinoma cells (HT29) and microglia cells (N9) to nanoplastics (25 nm, 50 nm, and 100 nm Polystyrene) to investigate their inflammatory responses, which are vital for body's defence. Although cytotoxicity remained generally low, HT29 cells exhibited a notable upregulation of p50 and p38 expression, concomitant with elevated TLR4 expression, in contrast with N9 cells that showed a less pronounced upregulation of these proteins. Additionally, nanoplastic exposure increased IL-1ß levels, partially attenuated by pre-exposure to TLR4 or p38 inhibitors. Intriguingly, N9 cells exposed to nanoplastics exhibited substantial increases in iNOS mRNA. This effect was entirely prevented by pre-exposure to TLR4 or p38 inhibitors, while TNF-α mRNA levels remained relatively stable. These findings underscore the potential of nanoplastics to activate inflammatory pathways, with response kinetics varying depending on the cell type.

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来源期刊
CiteScore
7.00
自引率
4.70%
发文量
185
审稿时长
34 days
期刊介绍: Environmental Toxicology and Pharmacology publishes the results of studies concerning toxic and pharmacological effects of (human and veterinary) drugs and of environmental contaminants in animals and man. Areas of special interest are: molecular mechanisms of toxicity, biotransformation and toxicokinetics (including toxicokinetic modelling), molecular, biochemical and physiological mechanisms explaining differences in sensitivity between species and individuals, the characterisation of pathophysiological models and mechanisms involved in the development of effects and the identification of biological markers that can be used to study exposure and effects in man and animals. In addition to full length papers, short communications, full-length reviews and mini-reviews, Environmental Toxicology and Pharmacology will publish in depth assessments of special problem areas. The latter publications may exceed the length of a full length paper three to fourfold. A basic requirement is that the assessments are made under the auspices of international groups of leading experts in the fields concerned. The information examined may either consist of data that were already published, or of new data that were obtained within the framework of collaborative research programmes. Provision is also made for the acceptance of minireviews on (classes of) compounds, toxicities or mechanisms, debating recent advances in rapidly developing fields that fall within the scope of the journal.
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