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尘肺是危害工人健康严重的职业病,包括种类多,涉及范围广,接触粉尘的人数多,对此各国均十分重视,并进行长期多方面的研究,尽管如此,就是其中危害最重的矽肺的发病机理,至今仍不完全清楚,其它尘肺则知道更少。1966年Allison等的研究指出,在肺组织里,矽尘被吞噬细胞吞噬后,吞噬细胞迅速出现死亡。Vigliani等提出的免疫学说是以吞噬细胞死亡为矽肺纤维化的起点。目前一些学者的研究认为矽尘吸入肺内,被其主要的靶细胞—巨噬细胞吞噬后,产生致纤维化因子,使成纤维细胞增生,胶元合成增多,引起肺部的纤维化过程,虽然具体事实尚待研究,但巨噬细胞在矽肺发病中所具有的作用,在矽肺研究中受到普遍重视。
Pneumoconiosis is a serious occupational disease that endangers the health of workers. It includes many kinds of diseases involving a large number of people exposed to dust. All countries attach great importance to this and carry out long-term and multi-faceted studies. However, the most serious of these is the incidence of silicosis The mechanism is still not fully understood yet, other pneumoconiosis know less. In 1966, Allison et al. Pointed out that in the lung tissue, phagocytes rapidly die after the silica dust is swallowed by phagocytes. Vigliani put forward the immune theory is the death of phagocytes as a starting point for silicosis. At present, some scholars believe that silica dust inhales into the lungs and is induced by fibroblasts, which are induced by its main target cell, macrophages. It causes fibroblasts to proliferate, increase the synthesis of collagen elements, cause fibrosis in the lungs, Although the specific facts to be studied, the role of macrophages in the pathogenesis of silicosis has received widespread attention in the study of silicosis.