COAL DUST EXPOSURE ON THE HUMAN PULMONARY ALVEOLAR MACROPHAGE

纤维性肺病发生在采矿业，原因是 矿工长期接触雾化矿物粉尘的研究 以煤和二氧化硅粉尘形式存在的粉尘颗粒。的相互作用 带有肺细胞的粉尘颗粒启动了一种病理生理 反应涉及肺泡巨噬细胞(AM)的释放 一种可以促进促炎的可溶性分泌产品 肺间质内的反应。我们的研究主要集中在 AM释放的炎性介质，如刺五加素， 白介素1β、肿瘤坏死因子和白介素6、一氧化氮与生长 矿物粉尘暴露后的TGFbeta等因素 了解肺纤维化的病理生理学，哪些粉尘 粒子是最具侵袭性的，并为早期制定可能的策略 简单煤工与复杂煤工的认知与内科治疗 尘肺病。我们已经描述了炎症性疾病的模式 介体释放(二十烷类化合物和细胞因子)与体外暴露 人肺泡巨噬细胞经支气管肺泡灌洗获得 矿物粉尘(煤和二氧化硅)，并最近检查了影响 二氧化硅暴露对TGFb合成和分泌反应的影响 一氧化氮和羟基自由基的形成。这项研究的特点是 进一步合成和释放TGFb，以确定TGFb的作用 肺泡巨噬细胞与肺之间相互作用中的细胞因子和二十烷类化合物 成纤维细胞与粉尘接触和检查之间的关系 AM中细胞内铁的沉积及其在AM中的作用 促进羟基和氧自由基的形成。AM细胞将会是 通过支气管肺泡灌洗从以下人类志愿者中获得 一个正常的人口和一个煤矿工人。

Fibrotic lung disease occurs in the mining industry as a result of chronic exposure of mine workers to mineral dust containing aerosolized dust particles in the form of coal and silica dusts. The interaction of the dust particle with cells of the lung initiates a pathophysiological response involving the pulmonary alveolar macrophage (AM with the release of soluble secretory products which can promote a proinflammatory response within the pulmonary interstitium. Our studies have focused on inflammatory mediators released by the AM such as the eciosanoids, cytokines including IL-1Beta, TNF and IL-6, nitric oxide and growth factors such as TGFBeta in response to mineral dust exposure to understand the pathophysiology of fibrotic lung disease, which dust particles are most invasive and to develop possible strategies for early recognition and medical therapy of simple and complicated coal workers pneumoconiosis. We have characterized the pattern of inflammatory mediator release (eicosanoids and cytokines) with in vitro exposure of human alveolar macrophages obtained through bronchoalveolar lavage to mineral dusts (coal and silica) and have recently examined the effects of silica exposure on the synthesis and secretory response of TGFB, nitric oxide and hydroxyl radical formation. This study characterizes further the synthesis and release of TGFB, to define the role of cytokines and eicosanoids in the interaction between the AM and the lung fibroblast with dust exposure and to examine the relationship between the deposition of intracellular iron in the AM and its potential for promoting hydroxyl and oxygen radical formation. AM cells will be harvested by bronchoalveolar lavage from human volunteers selected from a normal population and a population of coal miners.