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.
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