Lapp N L, Castranova V
Section of Pulmonary and Critical Care Medicine (NLL), West Virginia University Health Sciences Center, Morgantown 26506.
Occup Med. 1993 Jan-Mar;8(1):35-56.
In vitro and in vivo animal studies, as well as human investigations, strongly support the role of macrophage products in the development and progression of silicosis and coal workers' pneumoconiosis. Such products include enzymes and reactive oxygen species which may cause lung damage; cytokines which recruit and/or activate polymorphonuclear leukocytes and thus result in further oxidant damage to the lung; and fibrogenic factors which induce fibroblast proliferation and collagen synthesis. This mechanistic understanding of pulmonary disease should assist in developing strategies for prevention and treatment.
体外和体内动物研究以及人体研究都有力地支持了巨噬细胞产物在矽肺和煤工尘肺的发生和发展中所起的作用。这些产物包括可能导致肺损伤的酶和活性氧；可募集和/或激活多形核白细胞从而对肺造成进一步氧化损伤的细胞因子；以及诱导成纤维细胞增殖和胶原蛋白合成的纤维化因子。对肺部疾病的这种机制性理解应有助于制定预防和治疗策略。
