Induction of lung fibrosis in the mouse by intratracheal instillation of fluorescein isothiocyanate is not T-cell-dependent
Induction of lung fibrosis in the mouse by intratracheal instillation of fluorescein isothiocyanate is not T-cell-dependent
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DOI：
10.1016/s0002-9440(10)65493-4
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发表时间：
1999-11-01
影响因子：
6
通讯作者：
Toews, GB
中科院分区：
文献类型：
--
作者：
Christensen, PJ;Goodman, RE;Toews, GB
肺纤维化是多种损伤的病理结果。这组疾病的共同特征包括慢性炎症和免疫细胞激活。肺纤维化的发病机制还没有很好的定义，预后差，突出了需要良好的动物模型来阐明导致肺纤维化的细胞和分子事件。本文提供了一个新的肺纤维化模型的见解，使用一个单一的异硫氰酸荧光素（FITC）的肺内挑战。经皮注射FITC的Balb-c和C57 BL 6小鼠发生急性肺损伤，随后发生慢性炎症。与盐水处理的小鼠相比，在接种后第21天注意到肺胶原蛋白含量的显著增加。尽管特异性抗FITC血清抗体被废除，但与免疫活性对照组相比，T细胞缺陷动物的肺胶原蛋白含量出现相似的增加。因此，在FITC激发的小鼠中诱导纤维化不依赖于T细胞免疫。持续的慢性炎症和急性肺损伤可能是该模型中肺纤维化发展的诱发事件。
Pulmonary fibrosis is the pathological result of a diverse group of insults. Common features of this group of diseases include chronic inflammation and immune cell activation. The pathogenesis of pulmonary fibrosis is not well defined and the prognosis is poor, highlighting the need for good animal models to elucidate the cellular and molecular events that lead to pulmonary fibrosis. This paper provides insight on a newly described model of pulmonary fibrosis using a single intratracheal challenge with fluorescein isothiocyanate (FITC). Balb-c and C57BL6 mice given intratracheal FITC develop acute lung injury followed by chronic inflammation. Significant increases in lung collagen content compared to saline-treated mice are noted at day 21 after inoculation. T-cell-deficient animals develop similar increases in lung collagen content compared to immunocompetent controls despite the abrogation of specific anti-FITC serum antibodies. Thus, the induction of fibrosis in FITC-challenged mice is not dependent on T cell immunity. Persistent chronic inflammation and acute lung injury may be the inciting events for the development of lung fibrosis in this model.