期刊
INFECTION AND IMMUNITY
卷 69, 期 3, 页码 1889-1894出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.69.3.1889-1894.2001
关键词
-
资金
- NHLBI NIH HHS [HL36003, R01 HL036003, R37 HL036003] Funding Source: Medline
- NIA NIH HHS [AG13846, P30 AG013846] Funding Source: Medline
- NIDDK NIH HHS [DK52122] Funding Source: Medline
Hemolytic uremic syndrome (HUS) is associated with intestinal infection by enterohemorrhagic Escherichia coli strains that produce Shiga toxins. Globotriaosylceramide (Gb(3)) is the functional receptor for Shiga toxin, and tumor necrosis factor alpha (TNF-alpha) upregulates Gb(3) in both human macrovascular umbilical vein endothelial cells and human microvascular brain endothelial cells. TNF-alpha treatment enhanced Shiga toxin binding and sensitivity to toxin. This upregulation was specific for Gb(3) species containing normal fatty acids (NFA). Central nervous system (CNS) pathology in HUS could involve cytokine-stimulated elevation of endothelial NFA-Gb(3) levels. Differential expression of Gb(3) species may be a critical determinant of Shiga toxin toxicity and of CNS involvement in HUS.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据