Interleukin-17 and lipopolysaccharides synergistically induce cyclooxygenase-2 expression in human intestinal myofibroblasts

Zhuobin Zhang, Akira Andoh, Osamu Inatomi, Shigeki Bamba, Atsushi Takayanagi, Nobuyoshi Shimizu, Yoshihide Fujiyama

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Background: Colonic subepithelial myofibroblasts (SEMF) play a role in the modulation of mucosal inflammatory responses via the secretion of various inflammatory mediators. In the present study the effects of interleukin (IL)-17 and lipopolysaccharides (LPS) on cyclooxygenase (COX) expression in colonic SEMF were investigated. Methods: The expression of COX-1 and -2 proteins and mRNAs were determined by western and northern blotting, respectively. Nuclear factor (NF)-κB DNA binding activities were evaluated by electrophoretic gel mobility shift assays (EMSA). Results: The expression of COX-2 protein and mRNA was rapidly induced by the addition of IL-17 and LPS, whereas COX-1 expression was not affected by these factors. The effects of IL-17 and LPS were detected in a dose- and time-dependent manner. Furthermore, IL-17 and LPS synergistically induced COX-2 mRNA and protein expression. The EMSA demonstrated that the addition of IL-17 and LPS induced NF-κB activation within 1.5 h after stimulation, and a blockade of NF-κB activation by a recombinant adenovirus containing a stable form of IκBa markedly reduced the IL-17- and LPS-induced COX-2 mRNA expression. In these cells, the expression of Toll-like receptor (TLR)-4, which is a cellular receptor for LPS, was detected. Conclusion: Interleukin-17 and LPS play an important role in the induction of COX-2 in SEMF. These findings suggest that COX-2 expression and prostaglandin synthesis might be regulated by both T-cell-derived factor (IL-17) and bacterial products (LPS) in the inflamed mucosa.

Original languageEnglish
Pages (from-to)619-627
Number of pages9
JournalJournal of Gastroenterology and Hepatology (Australia)
Volume20
Issue number4
DOIs
Publication statusPublished - 2005

Fingerprint

Myofibroblasts
Interleukin-17
Cyclooxygenase 2
Lipopolysaccharides
Cyclooxygenase 1
Messenger RNA
Electrophoretic Mobility Shift Assay
Gels
CD14 Antigens
TCF Transcription Factors
Toll-Like Receptor 4
Proteins
Prostaglandin-Endoperoxide Synthases
Adenoviridae
Northern Blotting
Prostaglandins
Mucous Membrane
Western Blotting
DNA

Keywords

  • Bacteria
  • Cytokine
  • Cytoprotection
  • IBD

ASJC Scopus subject areas

  • Gastroenterology
  • Hepatology

Cite this

Interleukin-17 and lipopolysaccharides synergistically induce cyclooxygenase-2 expression in human intestinal myofibroblasts. / Zhang, Zhuobin; Andoh, Akira; Inatomi, Osamu; Bamba, Shigeki; Takayanagi, Atsushi; Shimizu, Nobuyoshi; Fujiyama, Yoshihide.

In: Journal of Gastroenterology and Hepatology (Australia), Vol. 20, No. 4, 2005, p. 619-627.

Research output: Contribution to journalArticle

Zhang, Zhuobin ; Andoh, Akira ; Inatomi, Osamu ; Bamba, Shigeki ; Takayanagi, Atsushi ; Shimizu, Nobuyoshi ; Fujiyama, Yoshihide. / Interleukin-17 and lipopolysaccharides synergistically induce cyclooxygenase-2 expression in human intestinal myofibroblasts. In: Journal of Gastroenterology and Hepatology (Australia). 2005 ; Vol. 20, No. 4. pp. 619-627.
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T1 - Interleukin-17 and lipopolysaccharides synergistically induce cyclooxygenase-2 expression in human intestinal myofibroblasts

AU - Zhang, Zhuobin

AU - Andoh, Akira

AU - Inatomi, Osamu

AU - Bamba, Shigeki

AU - Takayanagi, Atsushi

AU - Shimizu, Nobuyoshi

AU - Fujiyama, Yoshihide

PY - 2005

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N2 - Background: Colonic subepithelial myofibroblasts (SEMF) play a role in the modulation of mucosal inflammatory responses via the secretion of various inflammatory mediators. In the present study the effects of interleukin (IL)-17 and lipopolysaccharides (LPS) on cyclooxygenase (COX) expression in colonic SEMF were investigated. Methods: The expression of COX-1 and -2 proteins and mRNAs were determined by western and northern blotting, respectively. Nuclear factor (NF)-κB DNA binding activities were evaluated by electrophoretic gel mobility shift assays (EMSA). Results: The expression of COX-2 protein and mRNA was rapidly induced by the addition of IL-17 and LPS, whereas COX-1 expression was not affected by these factors. The effects of IL-17 and LPS were detected in a dose- and time-dependent manner. Furthermore, IL-17 and LPS synergistically induced COX-2 mRNA and protein expression. The EMSA demonstrated that the addition of IL-17 and LPS induced NF-κB activation within 1.5 h after stimulation, and a blockade of NF-κB activation by a recombinant adenovirus containing a stable form of IκBa markedly reduced the IL-17- and LPS-induced COX-2 mRNA expression. In these cells, the expression of Toll-like receptor (TLR)-4, which is a cellular receptor for LPS, was detected. Conclusion: Interleukin-17 and LPS play an important role in the induction of COX-2 in SEMF. These findings suggest that COX-2 expression and prostaglandin synthesis might be regulated by both T-cell-derived factor (IL-17) and bacterial products (LPS) in the inflamed mucosa.

AB - Background: Colonic subepithelial myofibroblasts (SEMF) play a role in the modulation of mucosal inflammatory responses via the secretion of various inflammatory mediators. In the present study the effects of interleukin (IL)-17 and lipopolysaccharides (LPS) on cyclooxygenase (COX) expression in colonic SEMF were investigated. Methods: The expression of COX-1 and -2 proteins and mRNAs were determined by western and northern blotting, respectively. Nuclear factor (NF)-κB DNA binding activities were evaluated by electrophoretic gel mobility shift assays (EMSA). Results: The expression of COX-2 protein and mRNA was rapidly induced by the addition of IL-17 and LPS, whereas COX-1 expression was not affected by these factors. The effects of IL-17 and LPS were detected in a dose- and time-dependent manner. Furthermore, IL-17 and LPS synergistically induced COX-2 mRNA and protein expression. The EMSA demonstrated that the addition of IL-17 and LPS induced NF-κB activation within 1.5 h after stimulation, and a blockade of NF-κB activation by a recombinant adenovirus containing a stable form of IκBa markedly reduced the IL-17- and LPS-induced COX-2 mRNA expression. In these cells, the expression of Toll-like receptor (TLR)-4, which is a cellular receptor for LPS, was detected. Conclusion: Interleukin-17 and LPS play an important role in the induction of COX-2 in SEMF. These findings suggest that COX-2 expression and prostaglandin synthesis might be regulated by both T-cell-derived factor (IL-17) and bacterial products (LPS) in the inflamed mucosa.

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