Premium
Lipopolysaccharide at low concentration suppressed tight junction assembly in intestinal epithelial cells via AMPK suppression and MAPK pathway
Author(s) -
Meesomboon Roojanaat,
Wongkrasant Preedajit,
Muanprasat Chatchai
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.710.1
Subject(s) - tight junction , ampk , lipopolysaccharide , mapk/erk pathway , western blot , chemistry , microbiology and biotechnology , intestinal permeability , occludin , phosphorylation , immunology , biology , protein kinase a , biochemistry , gene
Intestinal tight junction acts as a physical barrier and selective filter in intestine. Effect of low concentration of lipopolysaccharide (LPS) on AMPK activity, which is central to tight junction regulation, and its mechanism in intestinal epithelial cells (IEC) are not well characterized. This study aimed to investigate the effect of low‐concentration of LPS on AMPK suppression and intestinal tight junction permeability. To test whether low‐concentration of LPS inhibits AMPK phosphorylation, western blot analysis was performed. The result revealed that low dose LPS (1 ng/ml) suppresses AMPK activation in T84 cells. In order to investigate whether LPS suppressed intestinal tight junction assembly, calcium switch assays were performed. The result showed that LPS significantly suppressed tight junction assembly at 6 to 24 hours post‐treatment, indicating that low‐concentration of LPS inhibits tight junction assembly in IEC. Moreover, this effect was disappeared in the presence of U0126, a MAPK inhibitor. This data indicate that low‐concentration of LPS inhibits tight junction assembly via MAPK pathways. In conclusion, LPS induced AMPK suppression and tight junction permeability via MAPK pathway in IEC. This study shed light on the mechanism of intestinal diseases involving gram negative bacterial infection. Support or Funding Information This work is supported by Tonkla Ramathibodi program and Thailand Research Fund and Mahidol University. (BRG5980008) This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .