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首页> 外文期刊>International Journal of Environmental Research and Public Health >Fluoro-edenite Fibers Induce Expression of Hsp70 and Inflammatory Response
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Fluoro-edenite Fibers Induce Expression of Hsp70 and Inflammatory Response

机译：氟牙本质纤维诱导Hsp70的表达和炎症反应。

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Many asbestos-like mineral fibers have been detected in the air of mountainous and volcanic areas of Italy and other parts of the world. These fibers have been suspected to be the cause of increased incidences of lung cancer and other lung diseases in these areas. However, the mechanisms of the cellular response and defense following exposure to these microscopic fibers have not been characterized. We continue to study these mechanisms to be able to propose preventive strategies in large populations. The objective of the present study was to determine comparatively biological responses of mesothelial Met-5A and monocyte-macrophage J774 cells following exposure to two types of fluoro-edenite fibers having low and high iron content (labeled 19 and 27, respectively) obtained from Biancavilla (Sicily, Italy). The reference fiber was a non-iron fibrous tremolite from Val di Susa (Piemonte, Italy). The cells were treated with 5, 50, and 100 μg of fibrous matter per 1 ml for 72 hr. We identified several key mechanisms by which cells responded and counteracted the injury induced by these fibers. The fibers caused induction of the heat shock protein 70 (Hsp70), stimulated formation of reactive oxygen species (detected by using DCFH-DA as a fluorescent probe) and NO? (measured as nitrite). Exposure of cells to the fibers induced lactate dehydrogenase activity and decreased viability. The fluoro-endenite type 27 was the most potent fiber tested, which indicated that iron and possibly manganese contribute significantly to this fiber toxicity. The J774 cells were more sensitive to fluoro-edenite than Met-5A cells suggesting that the primary site of the fiberinduced inflammatory response could be the macrophage rather than the pulmonary epithelium. Fluoro-edenite produces more biological alterations with respect to non-iron tremolite. Hsp70 and free radicals could be important factors in the context of mineral fiber-induced acute lung injury leading possibly to mutagenic effects. We anticipate that pharmacological blockade of the fiber-dependent cellular responses could in long term offer preventive approach to combat lung diseases induced by these fibers.
机译：在意大利和世界其他地区的山区和火山地区的空气中，发现了许多类似石棉的矿物纤维。这些纤维被怀疑是这些地区肺癌和其他肺部疾病发病率上升的原因。但是，尚未发现暴露于这些微观纤维后的细胞反应和防御机制。我们将继续研究这些机制，以便能够在大范围人群中提出预防策略。本研究的目的是确定暴露于从比安卡维利亚获得的两种铁含量分别为低和高的氟-闪锌矿纤维（分别标记为19和27）后，间皮Met-5A和单核巨噬细胞J774细胞的相对生物学反应。 （意大利西西里岛）。参比纤维是购自Val di Susa（意大利Piemonte）的非铁纤维透闪石。每1 ml用5、50和100μg纤维状物质处理细胞72小时。我们确定了几种关键机制，通过这些机制，细胞可以响应并抵消这些纤维诱导的损伤。纤维引起热激蛋白70（Hsp70）的诱导，刺激了活性氧的形成（通过使用DCFH-DA作为荧光探针检测到）和NO？ （以亚硝酸盐计）。细胞暴露于纤维会诱导乳酸脱氢酶活性并降低活力。 27型氟-树胶是测试过的最有效的纤维，这表明铁和锰可能对该纤维的毒性有很大贡献。与Met-5A细胞相比，J774细胞对氟-辉石的敏感性更高，表明纤维诱导的炎症反应的主要部位可能是巨噬细胞而不是肺上皮。含氟辉石相对于非铁透闪石产生更多的生物学变化。在矿物纤维诱导的急性肺损伤中，Hsp70和自由基可能是重要因素，可能导致诱变作用。我们预期对纤维依赖性细胞应答的药理学阻断可长期提供预防方法，以对抗由这些纤维引起的肺部疾病。

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