Reduced apoptosis and ameliorated listeriosis in TRAIL-null mice
Reduced apoptosis and ameliorated listeriosis in TRAIL-null mice
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DOI：
10.4049/jimmunol.173.9.5652
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发表时间：
2004-11-01
影响因子：
4.4
通讯作者：
Chen, YHH
中科院分区：
文献类型：
--
作者：
Zheng, SJ;Jiang, J;Chen, YHH
李斯特菌病是一种由单核细胞增生李斯特菌引起的传染病。虽然细胞凋亡在李斯特菌病的发病机制中起着至关重要的作用，但李斯特菌病细胞死亡的分子机制仍有待确定。我们在这项研究中报道，缺乏TRAIL的小鼠对原发性李斯特菌病有部分抗性，用可溶性死亡受体5阻断TRAIL可显著改善该病。原发李斯特菌感染后，TRAIL（+/+）小鼠肝脏和脾脏中的李斯特菌数量是TRAIL（-/-）小鼠的10-100倍。这伴随着TRAIL（-/-）小鼠存活率的显著增加。TRAIL（-/-）小鼠淋巴细胞和髓细胞死亡明显受到抑制，导致脾脏明显增大。这些结果确定了TRAIL在李斯特菌病期间细胞凋亡中的关键作用。
Listeriosis is an infectious disease caused by the bacterium Listeria monocytogenes. Although it is well recognized that apoptosis plays a critical role in the pathogenesis of the disease, the molecular mechanisms of cell death in listeriosis remain to be established. We report in this study that mice deficient in TRAIL were partially resistant to primary listeriosis, and blocking TRAIL with a soluble death receptor 5 markedly ameliorated the disease. The numbers of Listeria in the liver and spleen of TRAIL(+/+) mice were 10-100 times greater than those in TRAIL(-/-) mice following primary Listeria infection. This was accompanied by a significant increase in the survival rate of TRAIL(-/-) mice. Lymphoid and myeloid cell death was significantly inhibited in TRAIL(-/-) mice, which led to marked enlargement of the spleen. These results establish a critical role for TRAIL in apoptosis during listeriosis.