Transmural pressure induces IL-6 secretion by intestinal epithelial cells
Article first published online: 28 JUN 2002
DOI: 10.1046/j.1365-2249.2002.01895.x
Additional Information
How to Cite
KISHIKAWA, H., MIURA, S., YOSHIDA, H., HIROKAWA, M., NAKAMIZO, H., HIGUCHI, H., ADACHI, M., NAKATSUMI, R. C., SUZUKI, H., SAITO, H. and ISHII, H. (2002), Transmural pressure induces IL-6 secretion by intestinal epithelial cells. Clinical & Experimental Immunology, 129: 86–91. doi: 10.1046/j.1365-2249.2002.01895.x
Publication History
- Issue published online: 28 JUN 2002
- Article first published online: 28 JUN 2002
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Keywords:
- intestinal epithelial cells IL-6 NF-κB NF-IL-6 transmural pressure
SUMMARY
Although intestinal epithelial cells (IECs) are known as an important source for IL-6, it is not known whether mechanical forces affect IL-6 production. We investigated how transmural pressure modulates IL-6 synthesis and activation of transcription factors in IECs. Pressure was loaded onto IEC-18 cells by introducing compressed helium gas into the cell culture flask for 1–48 h. IL-6 release into the culture media was determined by cell proliferation bioassay using an IL-6-dependent mouse hybridoma cell line (7TD1). Exposure to pressure (80 mmHg) significantly enhanced IL-6 release into the culture media from IEC-18 cells at 12 h. Under control conditions, IL-6 secretion was directed to the basolateral side, but after exposure to pressure IL-6 secretion was increased in both the apical and basolateral sides. A nuclear factor kappa B (NF-κB) decoy reversed completely the pressure-induced increase of IL-6 secretion by IEC-18 cells. Pressure treatment enhanced IL-6 mRNA expression in IECs within 6 h. Pressure loading significantly enhanced the activation of both NF-κB and NF-IL-6 from 1h in the nuclear protein of IEC-18 cells as assessed by the electrophoretic mobility shift assay using FITC-conjugated specific primers. Increased phosphorylation of I-kappa B was also demonstrated in the cytosol of IEC cells within 1h by Western blot analysis. These results suggest a possible role for pressure loading in immune modulation of the intestinal mucosa by the stimulation of IL-6 release from intestinal epithelial cells.

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