Anti-inflammatory effect of capsaicin in Helicobacter pylori-infected gastric epithelial cells

In Ohk Lee, Kwang Hyoung Lee, Jae Hee Pyo, Jie-Hyun Kim, Yeun Jung Choi, Yongchan Lee

Research output: Contribution to journalArticle

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Abstract

Background and aim: Capsaicin, the main pungent ingredient of hot red and chilli pepper, has been considered as not only a cytoprotective but also a detrimental agent to the gastric mucosa. However, the effect and mechanism of capsaicin that modulate the induction of pro-inflammatory cytokine in Helicobacter pylori-infected epithelial cells have not been investigated previously. Herein, we demonstrated that capsaicin inhibited the release of pro-inflammatory cytokine, interleukin-8 (IL-8) by H. pylori-infected gastric epithelial cells through nuclear factor-κB (NF-κB) signal pathway. Materials and methods: AGS or MKN45 cells as gastric epithelial cells and Vac A+, CagA+ wild-type H. pylori strain ATCC 49503 were used. Gastric epithelial cells were pre-treated with various concentrations of capsaicin and infected with H. pylori for different periods of time to determine IL-8 concentrations in culture supernatant by an ELISA assay. We measured IL-8 mRNA transcripts in H. pylori-infected gastric epithelial cells co-treated with capsaicin by reverse transcriptase-polymerase chain reaction analysis. We performed electrophoretic mobility shift assay to examine the NF-κB DNA binding activity with capsaicin and immunofluorescence microscopy to examine nuclear staining of p65. We also performed immunoblotting for IκB, IKK activity with capsaicin. Results: Capsaicin inhibits H. pylori-induced IL-8 production by gastric epithelial cells in dose- and time-dependent manner. Capsaicin as low as 100 μmol/L significantly inhibited IL-8 production in H. pylori-infected MKN45 cells (43.2% of control) at 24 hours incubation, whereas inhibited IL-8 production in H. pylori-infected AGS cells (70% of control). We confirmed that capsaicin inhibited IL-8 mRNA expression after infection of gastric epithelial cells with H. pylori for 6 hours. The addition of capsaicin (100 μmol/L) suppressed H. pylori-induced NF-κB activation in gastric epithelial cells at 1 hour post-infection. We also found that the degradation of IκB and IKK activation were inhibited by capsaicin. Conclusions: Nontoxic dose of capsaicin inhibited H. pylori-induced IL-8 production by gastric epithelial cells through the modulation of IκB-, NF-κB-, and IL-8 pathways. We conclude that capsaicin can be proposed as a potential anti-inflammatory drug by inhibition of the production of IL-8 in H. pylori-infected gastric epithelium.

Original languageEnglish
Pages (from-to)510-517
Number of pages8
JournalHelicobacter
Volume12
Issue number5
DOIs
Publication statusPublished - 2007 Oct 1

Fingerprint

Capsaicin
Helicobacter pylori
Stomach
Anti-Inflammatory Agents
Epithelial Cells
Interleukin-8
Capsicum
Cytokines
Messenger RNA
Electrophoretic Mobility Shift Assay
Gastric Mucosa
Infection
Reverse Transcriptase Polymerase Chain Reaction
Fluorescence Microscopy
Immunoblotting
Signal Transduction

All Science Journal Classification (ASJC) codes

  • Gastroenterology
  • Infectious Diseases

Cite this

Lee, In Ohk ; Lee, Kwang Hyoung ; Pyo, Jae Hee ; Kim, Jie-Hyun ; Choi, Yeun Jung ; Lee, Yongchan. / Anti-inflammatory effect of capsaicin in Helicobacter pylori-infected gastric epithelial cells. In: Helicobacter. 2007 ; Vol. 12, No. 5. pp. 510-517.
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title = "Anti-inflammatory effect of capsaicin in Helicobacter pylori-infected gastric epithelial cells",
abstract = "Background and aim: Capsaicin, the main pungent ingredient of hot red and chilli pepper, has been considered as not only a cytoprotective but also a detrimental agent to the gastric mucosa. However, the effect and mechanism of capsaicin that modulate the induction of pro-inflammatory cytokine in Helicobacter pylori-infected epithelial cells have not been investigated previously. Herein, we demonstrated that capsaicin inhibited the release of pro-inflammatory cytokine, interleukin-8 (IL-8) by H. pylori-infected gastric epithelial cells through nuclear factor-κB (NF-κB) signal pathway. Materials and methods: AGS or MKN45 cells as gastric epithelial cells and Vac A+, CagA+ wild-type H. pylori strain ATCC 49503 were used. Gastric epithelial cells were pre-treated with various concentrations of capsaicin and infected with H. pylori for different periods of time to determine IL-8 concentrations in culture supernatant by an ELISA assay. We measured IL-8 mRNA transcripts in H. pylori-infected gastric epithelial cells co-treated with capsaicin by reverse transcriptase-polymerase chain reaction analysis. We performed electrophoretic mobility shift assay to examine the NF-κB DNA binding activity with capsaicin and immunofluorescence microscopy to examine nuclear staining of p65. We also performed immunoblotting for IκB, IKK activity with capsaicin. Results: Capsaicin inhibits H. pylori-induced IL-8 production by gastric epithelial cells in dose- and time-dependent manner. Capsaicin as low as 100 μmol/L significantly inhibited IL-8 production in H. pylori-infected MKN45 cells (43.2{\%} of control) at 24 hours incubation, whereas inhibited IL-8 production in H. pylori-infected AGS cells (70{\%} of control). We confirmed that capsaicin inhibited IL-8 mRNA expression after infection of gastric epithelial cells with H. pylori for 6 hours. The addition of capsaicin (100 μmol/L) suppressed H. pylori-induced NF-κB activation in gastric epithelial cells at 1 hour post-infection. We also found that the degradation of IκB and IKK activation were inhibited by capsaicin. Conclusions: Nontoxic dose of capsaicin inhibited H. pylori-induced IL-8 production by gastric epithelial cells through the modulation of IκB-, NF-κB-, and IL-8 pathways. We conclude that capsaicin can be proposed as a potential anti-inflammatory drug by inhibition of the production of IL-8 in H. pylori-infected gastric epithelium.",
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Anti-inflammatory effect of capsaicin in Helicobacter pylori-infected gastric epithelial cells. / Lee, In Ohk; Lee, Kwang Hyoung; Pyo, Jae Hee; Kim, Jie-Hyun; Choi, Yeun Jung; Lee, Yongchan.

In: Helicobacter, Vol. 12, No. 5, 01.10.2007, p. 510-517.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Anti-inflammatory effect of capsaicin in Helicobacter pylori-infected gastric epithelial cells

AU - Lee, In Ohk

AU - Lee, Kwang Hyoung

AU - Pyo, Jae Hee

AU - Kim, Jie-Hyun

AU - Choi, Yeun Jung

AU - Lee, Yongchan

PY - 2007/10/1

Y1 - 2007/10/1

N2 - Background and aim: Capsaicin, the main pungent ingredient of hot red and chilli pepper, has been considered as not only a cytoprotective but also a detrimental agent to the gastric mucosa. However, the effect and mechanism of capsaicin that modulate the induction of pro-inflammatory cytokine in Helicobacter pylori-infected epithelial cells have not been investigated previously. Herein, we demonstrated that capsaicin inhibited the release of pro-inflammatory cytokine, interleukin-8 (IL-8) by H. pylori-infected gastric epithelial cells through nuclear factor-κB (NF-κB) signal pathway. Materials and methods: AGS or MKN45 cells as gastric epithelial cells and Vac A+, CagA+ wild-type H. pylori strain ATCC 49503 were used. Gastric epithelial cells were pre-treated with various concentrations of capsaicin and infected with H. pylori for different periods of time to determine IL-8 concentrations in culture supernatant by an ELISA assay. We measured IL-8 mRNA transcripts in H. pylori-infected gastric epithelial cells co-treated with capsaicin by reverse transcriptase-polymerase chain reaction analysis. We performed electrophoretic mobility shift assay to examine the NF-κB DNA binding activity with capsaicin and immunofluorescence microscopy to examine nuclear staining of p65. We also performed immunoblotting for IκB, IKK activity with capsaicin. Results: Capsaicin inhibits H. pylori-induced IL-8 production by gastric epithelial cells in dose- and time-dependent manner. Capsaicin as low as 100 μmol/L significantly inhibited IL-8 production in H. pylori-infected MKN45 cells (43.2% of control) at 24 hours incubation, whereas inhibited IL-8 production in H. pylori-infected AGS cells (70% of control). We confirmed that capsaicin inhibited IL-8 mRNA expression after infection of gastric epithelial cells with H. pylori for 6 hours. The addition of capsaicin (100 μmol/L) suppressed H. pylori-induced NF-κB activation in gastric epithelial cells at 1 hour post-infection. We also found that the degradation of IκB and IKK activation were inhibited by capsaicin. Conclusions: Nontoxic dose of capsaicin inhibited H. pylori-induced IL-8 production by gastric epithelial cells through the modulation of IκB-, NF-κB-, and IL-8 pathways. We conclude that capsaicin can be proposed as a potential anti-inflammatory drug by inhibition of the production of IL-8 in H. pylori-infected gastric epithelium.

AB - Background and aim: Capsaicin, the main pungent ingredient of hot red and chilli pepper, has been considered as not only a cytoprotective but also a detrimental agent to the gastric mucosa. However, the effect and mechanism of capsaicin that modulate the induction of pro-inflammatory cytokine in Helicobacter pylori-infected epithelial cells have not been investigated previously. Herein, we demonstrated that capsaicin inhibited the release of pro-inflammatory cytokine, interleukin-8 (IL-8) by H. pylori-infected gastric epithelial cells through nuclear factor-κB (NF-κB) signal pathway. Materials and methods: AGS or MKN45 cells as gastric epithelial cells and Vac A+, CagA+ wild-type H. pylori strain ATCC 49503 were used. Gastric epithelial cells were pre-treated with various concentrations of capsaicin and infected with H. pylori for different periods of time to determine IL-8 concentrations in culture supernatant by an ELISA assay. We measured IL-8 mRNA transcripts in H. pylori-infected gastric epithelial cells co-treated with capsaicin by reverse transcriptase-polymerase chain reaction analysis. We performed electrophoretic mobility shift assay to examine the NF-κB DNA binding activity with capsaicin and immunofluorescence microscopy to examine nuclear staining of p65. We also performed immunoblotting for IκB, IKK activity with capsaicin. Results: Capsaicin inhibits H. pylori-induced IL-8 production by gastric epithelial cells in dose- and time-dependent manner. Capsaicin as low as 100 μmol/L significantly inhibited IL-8 production in H. pylori-infected MKN45 cells (43.2% of control) at 24 hours incubation, whereas inhibited IL-8 production in H. pylori-infected AGS cells (70% of control). We confirmed that capsaicin inhibited IL-8 mRNA expression after infection of gastric epithelial cells with H. pylori for 6 hours. The addition of capsaicin (100 μmol/L) suppressed H. pylori-induced NF-κB activation in gastric epithelial cells at 1 hour post-infection. We also found that the degradation of IκB and IKK activation were inhibited by capsaicin. Conclusions: Nontoxic dose of capsaicin inhibited H. pylori-induced IL-8 production by gastric epithelial cells through the modulation of IκB-, NF-κB-, and IL-8 pathways. We conclude that capsaicin can be proposed as a potential anti-inflammatory drug by inhibition of the production of IL-8 in H. pylori-infected gastric epithelium.

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