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细菌脂多糖降低了肠屏障功能,并改变了IEC-6大鼠肠隐窝细胞中7H6抗原的定位。

Bacterial lipopolysaccharide reduced intestinal barrier function and altered localization of 7H6 antigen in IEC-6 rat intestinal crypt cells.

作者信息

Kimura H, Sawada N, Tobioka H, Isomura H, Kokai Y, Hirata K, Mori M

机构信息

Department of Pathology, Sapporo Medical University School of Medicine, Japan.

出版信息

J Cell Physiol. 1997 Jun;171(3):284-90. doi: 10.1002/(SICI)1097-4652(199706)171:3<284::AID-JCP6>3.0.CO;2-K.

Abstract

The intestinal epithelial barrier restricts the passage of potentially toxic substances into the systemic circulation and is considered to be mostly mediated by tight junctions, though the mechanisms involved in the regulation of intestinal tight junctions are not yet fully understood. In the present study, we examined whether bacterial lipopolysaccharide (LPS) altered the barrier function of tight junction and localization of tight junctional proteins, ZO-1 and 7H6 antigen, in IEC-6 intestinal cells. Administration of LPS to the basolateral surface of IEC-6 cells disrupted the barrier function and caused the disappearance of 7H6 antigen from the cell border, whereas LPS administered to the apical surface altered neither the barrier function nor the localization of 7H6 antigen in IEC-6 cells. On the other hand, the localization of ZO-1 was not influenced by these treatments of LPS. These results suggest that the interaction of LPS with the basolateral surface of intestinal epithelial cells disrupts the barrier function and 7H6 antigen take part in the maintenance of the barrier function in IEC-6 cells.

摘要

肠道上皮屏障限制潜在有毒物质进入体循环,其主要被认为是由紧密连接介导的,尽管肠道紧密连接的调节机制尚未完全明确。在本研究中,我们检测了细菌脂多糖(LPS)是否改变紧密连接的屏障功能以及紧密连接蛋白ZO-1和7H6抗原在IEC-6肠细胞中的定位。将LPS施加于IEC-6细胞的基底外侧表面会破坏屏障功能,并导致7H6抗原从细胞边界消失,而将LPS施加于顶端表面既不改变IEC-6细胞的屏障功能,也不改变7H6抗原的定位。另一方面,ZO-1的定位不受这些LPS处理的影响。这些结果表明,LPS与肠道上皮细胞基底外侧表面的相互作用会破坏屏障功能,并且7H6抗原参与IEC-6细胞中屏障功能的维持。

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