实验性矽肺不会加重小鼠胶原诱导的关节炎。

Robby Engelmann, Brigitte Müller-Hilke
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引用次数: 4

摘要

目的:探讨慢性肺部炎症对小鼠胶原性关节炎发病及严重程度的影响。方法:通过鼻内应用二氧化硅颗粒诱导慢性肺部炎症,表现为矽肺病。1周后开始用II型胶原蛋白免疫,6周后处死小鼠。此后,通过流式细胞术确诊矽肺病,并通过膝关节和足部组织学评估关节炎。结果:与pbs处理的对照组小鼠相比,二氧化硅处理小鼠明显的肺部炎症表现为支气管肺泡灌洗(BAL)细胞计数显著升高,这是由于巨噬细胞和粒细胞数量增加。肺部炎症与PAD2和PAD4表达升高无关,但二氧化硅处理动物的aCCP血清滴度显著升高。然而,肺部炎症并没有导致关节炎发病率的增加,也没有加重宏观或组织学关节评分。结论:矽肺引起的慢性肺部炎症不会加重小鼠胶原诱导的关节炎。
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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Experimental silicosis does not aggravate collagen-induced arthritis in mice.

Objectives: To investigate the effect of chronic lung inflammation on the incidence and severity of collagen-induced arthritis in mice.

Methods: Chronic lung inflammation in the form of silicosis was induced via intranasal application of silica particles. Immunization with collagen Type II commenced one week later and mice were sacrificed six weeks after booster immunization. Thereafter, silicosis was confirmed via flow cytometry and arthritis was evaluated performing knee and paw histology.

Results: Pronounced lung inflammation in the silica-treated compared to PBS-treated control mice was demonstrated by significantly elevated broncho-alveolar lavage (BAL) cell count, attributable to increased numbers of macrophages and granulocytes. Inflammation in the lungs was not associated with elevated PAD2 and PAD4 expression, yet silica treated animals had significantly higher aCCP serum titers. However, lung inflammation did not lead to an increase in the incidence of arthritis, nor did it exacerbate the macroscopic or histologic joint scores.

Conclusions: Chronic lung inflammation resulting from silicosis does not aggravate collagen-induced arthritis in mice.

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