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Fipronil upregulates inflammatory cytokines and MUC5AC expression in human nasal epithelial cells.

氟虫腈上调人鼻上皮细胞炎症细胞因子和 MUC5AC 的表达。

  • 影响因子:2.88
  • DOI:10.4193/Rhin19.172
  • 作者列表:"Kwak S","Choi YS","Na HG","Bae CH","Song SY","Kim YD
  • 发表时间:2020-02-01
Abstract

BACKGROUND:Airway inflammation and excessive mucin production are pathophysiological characteristics of airway diseases. Fipronil, a pesticide, is being extensively used in agriculture and veterinary medicine worldwide. However, this compound impairs immune function in non-target organisms. The present study aimed to evaluate the effect of fipronil on pro-inflammatory cytokine and mucus production and signalling pathways in human primary nasal METHODOLOGY: The effect of fipronil on pro-inflammatory cytokine and MUC5AC expression and the signalling pathway of fipronil were investigated using real-time PCR, enzyme immunoassays, immunofluorescence, and immunoblot analysis with specific inhibitors and small interfering RNA. RESULTS:Fipronil treatment increased pro-inflammatory cytokine interleukin (IL)-1beta, IL-6, IL-8, and MUC5AC expression in human primary nasal epithelial cells. It also induced phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) mitogenactivated protein kinase (MAPK), p38 MAPK, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB). MAPK and NF-kB inhibitor treatment significantly inhibited increases in IL-1beta, IL-6, IL-8, and MUC5AC expression. Ex vivo data confirmed that fipronil-induced MUC5AC expression occurs through ERK1/2, p38, and NF-kB signalling pathways in nasal inferior turbinate tissue. CONCLUSIONS:Fipronil induced pro-inflammatory cytokine IL-1beta, IL-6, IL-8, and MUC5AC expression via ERK1/2 MAPK, p38 MAPK, and NF-kB in human primary nasal epithelial cells.

摘要

背景: 气道炎症和黏蛋白生成过多是气道疾病的病理生理特征。氟虫腈是一种杀虫剂,在世界范围内广泛用于农业和兽医。然而,这种化合物损害了非靶生物的免疫功能。本研究旨在评价氟虫腈对人原发性鼻方法学中促炎细胞因子和粘液产生及信号通路的影响: 采用实时荧光定量 PCR 、酶免疫、免疫荧光、荧光等方法研究了氟虫腈对促炎细胞因子和 MUC5AC 表达的影响及氟虫腈的信号通路,并用特异性抑制剂和小干扰 RNA 进行免疫印迹分析。 结果: 氟虫腈处理可增加人鼻黏膜上皮细胞中促炎细胞因子白细胞介素 (IL)-1 β 、 IL-6 、 IL-8 和 MUC5AC 的表达。它还诱导细胞外信号调节激酶 1/2 (ERK1/2) 有丝分裂原激活蛋白激酶 (MAPK) 的磷酸化,p38 MAPK, 和活化 B 细胞的核因子 κ 轻链增强子 (NF-kB)。MAPK 和 NF-kB 抑制剂处理显著抑制 IL-1beta 、 IL-6 、 IL-8 和 MUC5AC 表达的增加。离体数据证实,氟虫腈诱导的 MUC5AC 表达通过下鼻甲组织中的 ERK1/2 、 p38 和 NF-kB 信号通路发生。 结论: 氟虫腈可通过 ERK1/2 MAPK 、 p38 MAPK 和 NF-kB 诱导人鼻黏膜上皮细胞 IL-1beta 、 IL-6 、 IL-8 和 MUC5AC 的表达。

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影响因子:3.94
发表时间:2020-01-15
DOI:10.1016/j.taap.2019.114847
作者列表:["Bernstein DM","Toth B","Rogers RA","Kling DE","Kunzendorf P","Phillips JI","Ernst H"]

METHODS::The interim results from this 90-day multi-dose, inhalation toxicology study with life-time post-exposure observation has shown an important fundamental difference in persistence and pathological response in the lung between brake dust derived from brake-pads manufactured with chrysotile, TiO2 or chrysotile alone in comparison to the amphiboles, crocidolite and amosite asbestos. In the brake dust exposure groups no significant pathological response was observed at any time. Slight macrophage accumulation of particles was noted. Wagner-scores, were from 1 to 2 (1 = air-control group) and were similar to the TiO2 group. Chrysotile being biodegradable, shows a weakening of its matrix and breaking into short fibers & particles that can be cleared by alveolar macrophages and continued dissolution. In the chrysotile exposure groups, particle laden macrophage accumulation was noted leading to a slight interstitial inflammatory response (Wagner-score 1-3). There was no peribronchiolar inflammation and occasional very slight interstitial fibrosis. The histopathology and the confocal analyses clearly differentiate the pathological response from amphibole asbestos, crocidolite and amosite, compared to that from the brake dust and chrysotile. Both crocidolite and amosite induced persistent inflammation, microgranulomas, and fibrosis (Wagner-scores 4), which persisted through the post exposure period. The confocal microscopy of the lung and snap-frozen chestwalls quantified the extensive inflammatory response and collagen development in the lung and on the visceral and parietal surfaces. The interim results reported here, provide a clear basis for differentiating the effects from brake dust exposure from those following amphibole asbestos exposure. The subsequent results through life-time post-exposure will follow.

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影响因子:4.04
发表时间:2020-01-10
DOI:10.1042/BST20191010
作者列表:["Zaragosi LE","Deprez M","Barbry P"]

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