Apoptotic and inflammatory signaling via Fas and tumor necrosis factor receptor I contribute to the development of chest trauma-induced septic acute lung injury
Apoptotic and inflammatory signaling via Fas and tumor necrosis factor receptor I contribute to the development of chest trauma-induced septic acute lung injury
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通过 Fas 和肿瘤坏死因子受体 I 的细胞凋亡和炎症信号传导导致胸部创伤引起的脓毒症急性肺损伤的发生
DOI：
10.1097/ta.0b013e31827a3655
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发表时间：
2013
影响因子：
3.4
通讯作者：
Perl M
中科院分区：
文献类型：
--
作者：
Weckbach S;Hohmann C;Denk S;Kellermann P;Huber-Lang MS;Baumann B;Wirth T;Gebhard F;Bachem M;Perl M
直接急性肺损伤（ALI）仍然与高死亡率相关，而其潜在的病理机制尚未完全了解。在这方面，肺中的上皮细胞死亡已被认为在该临床实体的发病机制中起重要作用。基于此背景，我们假设通过Fas和肿瘤坏死因子受体1（TNFR-1）的信号传导参与介导胸部创伤诱导的脓毒性ALI中的细胞凋亡和炎症。MRL-Faslpr/J [lpr]）（lpr）和雄性TNFR-1缺陷小鼠（TNFR-1−/−）进行直接ALI模型，该模型包括钝性胸部创伤，随后盲肠结扎和穿刺。
BACKGROUNDDirect acute lung injury (ALI) is still associated with a high mortality, whereas the underlying pathomechanisms are not yet fully understood. In this regard, epithelial cell death in the lungs has been attributed an important role in the pathogenesis of this clinical entity. Based on this background here, we hypothesized that signaling through Fas and tumor necrosis factor receptor 1 (TNFR-1) is involved in mediating apoptosis and inflammation in chest trauma induced septic ALI.METHODSMale C57BL/6 mice (wild-type [WT]), male mutant mice expressing nonfunctional Fas receptor (B6. MRL-Faslpr/J [lpr])(lpr) and male TNFR-1–deficient mice (TNFR-1−/−) were subjected to a model of direct ALI consisting of blunt chest trauma followed by cecal ligation and puncture.
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影响因子：
8.8
作者：
Goss, CH;Brower, RG;Rubenfeld, GD
通讯作者：
Rubenfeld, GD
影响因子：
4.3
作者：
Sheikh, M. Saeed;Huang, Ying
通讯作者：
Huang, Ying
影响因子：
8.8
作者：
Perl, M;Gebhard, F;Knöferl, MW
通讯作者：
Knöferl, MW
影响因子：
3.1
作者：
Knöferl, MW;Liener, UC;Gebhard, F
通讯作者：
Gebhard, F
影响因子：
56.9
作者：
Grassmé, H;Kirschnek, S;Gulbins, E
通讯作者：
Gulbins, E