Davies R, Erdogdu G
MRC Toxicology Unit, Carshalton, Surrey, United Kingdom.
Exp Lung Res. 1989 Mar;15(2):285-97. doi: 10.3109/01902148909087859.
The in vitro secretion of fibronectin by rat alveolar macrophages recovered following the intratracheal instillation of various mineral dusts was examined using a competitive enzyme-linked immunoassay (CELIA) method. Cells derived with the fibrogenic dusts DQ12 quartz and UICC crocidolite asbestos had elevated rates of fibronectin secretion when compared ith those derived from titanium dioxide or saline. The in vitro culture of alveolar macrophages with dusts did not lead to elevated rates of fibronectin secretion, suggesting that mechanisms other than the direct interaction between dusts and macrophages may be responsible for elevated rates of fibronectin secretion by cells exposed to fibrogenic dusts. This suggests that fibronectin deposition seen in pneumoconiotic lesions in immunohistochemical studies may in part have been derived from macrophages. Thioglycollate-induced activated mouse peritoneal macrophages secreted significantly less fibronectin than resident peritoneal macrophages, a finding contrasting with those of Tsukamoto et al. [7].
采用竞争性酶联免疫分析（CELIA）方法，检测经气管内滴注各种矿物粉尘后大鼠肺泡巨噬细胞体外纤连蛋白的分泌情况。与源自二氧化钛或生理盐水的细胞相比，源自致纤维化粉尘DQ12石英和国际癌症研究机构（UICC）青石棉的细胞，其纤连蛋白分泌率升高。用粉尘对肺泡巨噬细胞进行体外培养，并未导致纤连蛋白分泌率升高，这表明除了粉尘与巨噬细胞之间的直接相互作用外，其他机制可能是接触致纤维化粉尘的细胞纤连蛋白分泌率升高的原因。这表明免疫组织化学研究中在尘肺病变中所见的纤连蛋白沉积，可能部分源自巨噬细胞。巯基乙酸盐诱导激活的小鼠腹腔巨噬细胞分泌的纤连蛋白明显少于常驻腹腔巨噬细胞，这一发现与冢本等人的研究结果相反[7]。
