Suppr超能文献

肿瘤坏死因子/淋巴毒素α双缺陷小鼠对博来霉素诱导的纤维化的抗性

Resistance of TNF/LT alpha double deficient mice to bleomycin-induced fibrosis.

作者信息

Piguet P F, Kaufman S, Barazzone C, Muller M, Ryffel B, Eugster H P

机构信息

Amgen Inc, Thousand Oaks, Ca 91320, USA.

出版信息

Int J Exp Pathol. 1997 Feb;78(1):43-8. doi: 10.1046/j.1365-2613.1997.d01-240.x.

Abstract

In order to evaluate the role and mode of action of TNF in bleomycin-induced lung fibrosis, mice deficient for TNF and LT alpha (delta TNF/LT alpha) were examined at 2 months of age and after 3 weekly i.v. injections of bleomycin. The body weight of the delta TNF/LT alpha mice was 88 +/- 11% of that of the wild type littermates. Lung collagen, evaluated by its hydroxyproline content, was also lower (81 +/- 9%) in mutant than in wild type littermates. Bleomycin induced a diffuse alveolitis with focal areas of alveolar remodelling in wild type but not in delta TNF/LT alpha, mice. Lymphoid infiltration was also prominent in wild type, but absent from delta TNF/LT alpha, mice. Bleomycin injections increased collagen deposition, as evaluated by the lung hydroxyproline content, more markedly in wild type, than in delta TNF/LT alpha, mice. Cell trapping in the alveolar capillaries was evaluated by semi-quantitative electron microscopy. Bleomycin markedly increased platelet trapping in the alveolar capillaries of wild type, but not of delta TNF/LT alpha, mice. This study indicates that the expression of TNF/LT alpha genes increases the deposition of collagen in both untreated and inflamed lung and that these genes may act, at least in part, by promoting platelet trapping.

摘要

为了评估肿瘤坏死因子(TNF)在博来霉素诱导的肺纤维化中的作用及作用方式,对缺乏TNF和淋巴毒素α(ΔTNF/LTα)的小鼠在2月龄时以及经静脉每周注射一次博来霉素共3周后进行了检查。ΔTNF/LTα小鼠的体重为野生型同窝小鼠体重的88±11%。通过羟脯氨酸含量评估的肺胶原蛋白含量,突变小鼠也低于野生型同窝小鼠(81±9%)。博来霉素在野生型小鼠中诱导了弥漫性肺泡炎,并伴有局部肺泡重塑区域,但在ΔTNF/LTα小鼠中未出现。野生型小鼠中淋巴细胞浸润也很明显,但ΔTNF/LTα小鼠中没有。通过肺羟脯氨酸含量评估,博来霉素注射后野生型小鼠的胶原蛋白沉积增加比ΔTNF/LTα小鼠更明显。通过半定量电子显微镜评估肺泡毛细血管中的细胞滞留情况。博来霉素显著增加了野生型小鼠肺泡毛细血管中的血小板滞留,但在ΔTNF/LTα小鼠中未出现。这项研究表明,TNF/LTα基因的表达增加了未处理和炎症肺中的胶原蛋白沉积,并且这些基因可能至少部分地通过促进血小板滞留起作用。

相似文献

引用本文的文献

9
Lung fibrosis.肺纤维化
Springer Semin Immunopathol. 1999;21(4):453-74. doi: 10.1007/s002810000036.
10
Interstitial fibrosis and growth factors.间质纤维化与生长因子
Environ Health Perspect. 2000 Aug;108 Suppl 4(Suppl 4):751-62. doi: 10.1289/ehp.00108s4751.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验