Cutting edge: Bacterial modulation of epithelial signaling via changes in neddylation of cullin-1
Cutting edge: Bacterial modulation of epithelial signaling via changes in neddylation of cullin-1
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DOI：
10.4049/jimmunol.175.7.4194
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发表时间：
2005-10-01
影响因子：
4.4
通讯作者：
Neish, AS
中科院分区：
文献类型：
--
作者：
Collier-Hyams, LS;Sloane, V;Neish, AS
人类肠道植物群在肠道健康和疾病中起着重要作用。某些肠道细菌可以通过阻断I κ B-α泛素化来抑制NF-κ B途径。I κ B-α泛素化由E3-SCF β TrCP泛素连接酶催化，其本身通过泛素样蛋白NEDD 8共价修饰cullin-1亚基来调节。neddylation是一种与细胞信号传导相关的多种细胞过程相关的生化事件，然而，在哺乳动物系统中尚未描述cullin neddylation的生理调节。我们报道了非致病性细菌与上皮细胞的相互作用导致neddylated Cul-1的快速丢失和随后NF-κ B途径的抑制。这一观察结果可以解释肠道细菌群落影响不同真核生物过程的能力，特别是哺乳动物肠上皮细胞的炎症耐受性。
The human enteric flora plays a significant role in intestinal health and disease. Certain enteric bacteria can inhibit the NF-kappa B pathway by blockade of I kappa B-alpha ubiquitination. I kappa B-alpha ubiquitination is catalyzed by the E3-SCF beta TrCP ubiquitin ligase, which is itself regulated via covalent modification of the cullin-1 subunit by the ubiquitin-like protein NEDD8. Neddaylation is a biochemical event associated with diverse cellular processes related to cell signaling, however, physiological regulation of cullin neddylation has not been described in mammalian systems. We report that interaction of nonpathogenic bacteria with epithelial cells resulted in a rapid loss of neddylated Cul-1 and consequent repression of the NF-kappa B pathway. This observation may explain the ability of intestinal bacterial communities to influence diverse eukaryotic processes in general and inflammatory tolerance of the mammalian intestinal epithelia specifically.