αpix interacts with Helicobacter pylori CagA to induce IL-8 expression in gastric epithelial cells

Joo Weon Lim, Kyung Hwan Kim, Hye Young Kim

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Objective.Helicobacter pylori CagA, translocated into gastric epithelial cells, induces IL-8 expression through the signalling pathways, including extracellular signal-regulated kinase (ERK) and nuclear factor-κB (NF-κB). We previously demonstrated that CagA interacts with host αPix. The present study was purposed to determine the role of the interaction of αPix with CagA on the signalling pathways for IL-8 expression in H. pylori-infected gastric epithelial cells. Material and methods.H. pylori HP99 strain (CagA+, VacA + ) was infected to gastric epithelial AGS cells transfected with non-targeting (NT) or αPix- targeting siRNA. Activation of signalling molecules including p21-activated kinase (PAK), ERK and NF-κB, and expression of IL-8 in the cells were assessed. Results:H. pylori CagA was delivered into AGS cells and then interacted with αPix at 4 h following H. pylori infection. PAK1, ERK and NF-κB were activated in the cells containing NT and αPix siRNA at 12 h following H. pylori infection. However, after 4 h, the time when CagA was delivered into the cells, the activations of PAK1, ERK and NF-κB were inhibited by down-regulation of αPix using siRNA but not by NT siRNA. The results indicate that αPix is required for H. pylori-mediated signalling of PAK1, ERK and NF-B. Additionally, Pix siRNA suppressed IL-8 induction after translocation of CagA into the cells, indicating that interaction of CagA with Pix is critical for CagA-mediating signalling for IL-8 expression. Conclusions. The interaction of αPix with CagA activates PAK1, ERK and NF-κB, which induces IL-8 expression in H. pylori-infected gastric epithelial cells.

Original languageEnglish
Pages (from-to)1166-1172
Number of pages7
JournalScandinavian Journal of Gastroenterology
Volume44
Issue number10
DOIs
Publication statusPublished - 2009 Nov 9

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Interleukin-8
Helicobacter pylori
Stomach
Extracellular Signal-Regulated MAP Kinases
Epithelial Cells
Small Interfering RNA
Helicobacter Infections
p21-Activated Kinases
Cell Communication
Down-Regulation

All Science Journal Classification (ASJC) codes

  • Gastroenterology

Cite this

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title = "αpix interacts with Helicobacter pylori CagA to induce IL-8 expression in gastric epithelial cells",
abstract = "Objective.Helicobacter pylori CagA, translocated into gastric epithelial cells, induces IL-8 expression through the signalling pathways, including extracellular signal-regulated kinase (ERK) and nuclear factor-κB (NF-κB). We previously demonstrated that CagA interacts with host αPix. The present study was purposed to determine the role of the interaction of αPix with CagA on the signalling pathways for IL-8 expression in H. pylori-infected gastric epithelial cells. Material and methods.H. pylori HP99 strain (CagA+, VacA + ) was infected to gastric epithelial AGS cells transfected with non-targeting (NT) or αPix- targeting siRNA. Activation of signalling molecules including p21-activated kinase (PAK), ERK and NF-κB, and expression of IL-8 in the cells were assessed. Results:H. pylori CagA was delivered into AGS cells and then interacted with αPix at 4 h following H. pylori infection. PAK1, ERK and NF-κB were activated in the cells containing NT and αPix siRNA at 12 h following H. pylori infection. However, after 4 h, the time when CagA was delivered into the cells, the activations of PAK1, ERK and NF-κB were inhibited by down-regulation of αPix using siRNA but not by NT siRNA. The results indicate that αPix is required for H. pylori-mediated signalling of PAK1, ERK and NF-B. Additionally, Pix siRNA suppressed IL-8 induction after translocation of CagA into the cells, indicating that interaction of CagA with Pix is critical for CagA-mediating signalling for IL-8 expression. Conclusions. The interaction of αPix with CagA activates PAK1, ERK and NF-κB, which induces IL-8 expression in H. pylori-infected gastric epithelial cells.",
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αpix interacts with Helicobacter pylori CagA to induce IL-8 expression in gastric epithelial cells. / Lim, Joo Weon; Kim, Kyung Hwan; Kim, Hye Young.

In: Scandinavian Journal of Gastroenterology, Vol. 44, No. 10, 09.11.2009, p. 1166-1172.

Research output: Contribution to journalArticle

TY - JOUR

T1 - αpix interacts with Helicobacter pylori CagA to induce IL-8 expression in gastric epithelial cells

AU - Lim, Joo Weon

AU - Kim, Kyung Hwan

AU - Kim, Hye Young

PY - 2009/11/9

Y1 - 2009/11/9

N2 - Objective.Helicobacter pylori CagA, translocated into gastric epithelial cells, induces IL-8 expression through the signalling pathways, including extracellular signal-regulated kinase (ERK) and nuclear factor-κB (NF-κB). We previously demonstrated that CagA interacts with host αPix. The present study was purposed to determine the role of the interaction of αPix with CagA on the signalling pathways for IL-8 expression in H. pylori-infected gastric epithelial cells. Material and methods.H. pylori HP99 strain (CagA+, VacA + ) was infected to gastric epithelial AGS cells transfected with non-targeting (NT) or αPix- targeting siRNA. Activation of signalling molecules including p21-activated kinase (PAK), ERK and NF-κB, and expression of IL-8 in the cells were assessed. Results:H. pylori CagA was delivered into AGS cells and then interacted with αPix at 4 h following H. pylori infection. PAK1, ERK and NF-κB were activated in the cells containing NT and αPix siRNA at 12 h following H. pylori infection. However, after 4 h, the time when CagA was delivered into the cells, the activations of PAK1, ERK and NF-κB were inhibited by down-regulation of αPix using siRNA but not by NT siRNA. The results indicate that αPix is required for H. pylori-mediated signalling of PAK1, ERK and NF-B. Additionally, Pix siRNA suppressed IL-8 induction after translocation of CagA into the cells, indicating that interaction of CagA with Pix is critical for CagA-mediating signalling for IL-8 expression. Conclusions. The interaction of αPix with CagA activates PAK1, ERK and NF-κB, which induces IL-8 expression in H. pylori-infected gastric epithelial cells.

AB - Objective.Helicobacter pylori CagA, translocated into gastric epithelial cells, induces IL-8 expression through the signalling pathways, including extracellular signal-regulated kinase (ERK) and nuclear factor-κB (NF-κB). We previously demonstrated that CagA interacts with host αPix. The present study was purposed to determine the role of the interaction of αPix with CagA on the signalling pathways for IL-8 expression in H. pylori-infected gastric epithelial cells. Material and methods.H. pylori HP99 strain (CagA+, VacA + ) was infected to gastric epithelial AGS cells transfected with non-targeting (NT) or αPix- targeting siRNA. Activation of signalling molecules including p21-activated kinase (PAK), ERK and NF-κB, and expression of IL-8 in the cells were assessed. Results:H. pylori CagA was delivered into AGS cells and then interacted with αPix at 4 h following H. pylori infection. PAK1, ERK and NF-κB were activated in the cells containing NT and αPix siRNA at 12 h following H. pylori infection. However, after 4 h, the time when CagA was delivered into the cells, the activations of PAK1, ERK and NF-κB were inhibited by down-regulation of αPix using siRNA but not by NT siRNA. The results indicate that αPix is required for H. pylori-mediated signalling of PAK1, ERK and NF-B. Additionally, Pix siRNA suppressed IL-8 induction after translocation of CagA into the cells, indicating that interaction of CagA with Pix is critical for CagA-mediating signalling for IL-8 expression. Conclusions. The interaction of αPix with CagA activates PAK1, ERK and NF-κB, which induces IL-8 expression in H. pylori-infected gastric epithelial cells.

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