Induction of dermal and subcutaneous inflammation by recombinant cachectin/tumor necrosis factor (TNF alpha) in the mouse.
Induction of dermal and subcutaneous inflammation by recombinant cachectin/tumor necrosis factor (TNF alpha) in the mouse.
复制标题
重组恶病质素/肿瘤坏死因子 (TNF α) 在小鼠体内诱导真皮和皮下炎症。
DOI：
10.1111/1523-1747.ep12475754
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Granstein,RD
中科院分区：
文献类型：
--
作者：
Sharpe,RJ;Margolis,RJ;Askari,M;Amento,EP;Granstein,RD
在小鼠模型上观察了恶病质/肿瘤坏死因子(肿瘤坏死因子-α)诱导急性皮肤和皮下炎症的能力。一些其他蛋白质和单独的稀释剂被检测作为对照。重组人肿瘤坏死因子α(rHuTNFα)经小鼠足底皮下注射后，3h开始出现明显的炎症反应，4~2 4h达高峰，79h消退，重组白细胞介素2、细胞色素c和热灭活的rHuTNFα可忽略不同程度的炎症反应。重组人淋巴毒素(肿瘤坏死因子β)，另一个控制蛋白，也引起了我们的系统急性炎症。由于与肿瘤坏死因子α和肿瘤坏死因子β部分同源，它们可能通过相似的机制发挥作用。肿瘤坏死因子α的这种促炎作用可能源于趋化活性，也可能是通过诱导次级介质。消炎痛可部分抑制肿瘤坏死因子α诱导的炎症反应，提示环氧合酶途径的产物可能参与了炎症反应的一部分。每天向小鼠足垫注射5次rHuTNFα可导致以单核细胞为主的浸润性病变和局灶性纤维化。这些结果提示，肿瘤坏死因子α可能是体内急性炎症的重要介质，并可能为胶原的产生提供信号。
The ability of cachectin/tumor necrosis factor (TNFα) to induce acute dermal and subcutaneous inflammation was examined in a murine model. A number of other proteins, and diluent alone were examined as controls. After subcutaneous injection into the mouse footpad, recombinant human TNFα(rHuTNFα) induced acute inflammation with an initial marked dermal and subcutaneous neutrophil infiltrate by approximately 3 h, with a peak between 4 and 24 h and resolution by 79 h. Recombinant interleukin-2, cytochrome c, and heat-inactivated rHuTNFα induced negligible inflammation. Recombinant human lymphotoxin (TNFβ), another control protein, also induced acute inflammation in our system. Because and TNFα and TNFβ are partially homologous, they may be acting through a similar mechanism. This pro-inflammatory effect of TNFα may result from chemotactic activity as well as by induction of secondary mediators. Inflammation induced by TNFα was partially suppressed by indomethacin treatment, suggesting that products of the cyclo-oxyganase pathway may mediate a portion of the inflammation involved. Five daily injections of rHuTNFα into the mouse footpad resulted in a predominantly mononuclear infiltrate and focal fibrosis. These results suggest that TNFα may be an important mediator of acute inflammation in vivo and might provide a signal for the production of collagen.