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Bacterial lipopolysaccharide reduced intestinal barrier function and altered localization of 7H6 antigen in IEC‐6 rat intestinal crypt cells
Author(s) -
Kimura Hiromichi,
Sawada Norimasa,
Tobioka Hirotoshi,
Isomura Hiroshi,
Kokai Yasuo,
Hirata Koichi,
Mori Michio
Publication year - 1997
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199706)171:3<284::aid-jcp6>3.0.co;2-k
Subject(s) - tight junction , barrier function , lipopolysaccharide , microbiology and biotechnology , antigen , crypt , microfold cell , intestinal epithelium , chemistry , function (biology) , epithelium , biology , immunology , endocrinology , genetics
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. J. Cell. Physiol. 171:284–290, 1997. © 1997 Wiley‐Liss, Inc.

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