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Jak1/Stat3 Is an Upstream Signaling of NF-κB Activation in Helicobacter pylori-Induced IL-8 Production in Gastric Epithelial AGS Cells
Helicobacter pylori (H. pylori) induces the activation of nuclear factor-kB (NF-κB) and cytokine expression in gastric epithelial cells. The Janus kinase/signal transducers and activators of transcription (Jak/Stat) cascade is the inflammatory signaling in various cells. The purpose of the present s...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Yonsei University College of Medicine
2015
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4397461/ https://www.ncbi.nlm.nih.gov/pubmed/25837197 http://dx.doi.org/10.3349/ymj.2015.56.3.862 |
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author | Cha, Boram Lim, Joo Weon Kim, Hyeyoung |
author_facet | Cha, Boram Lim, Joo Weon Kim, Hyeyoung |
author_sort | Cha, Boram |
collection | PubMed |
description | Helicobacter pylori (H. pylori) induces the activation of nuclear factor-kB (NF-κB) and cytokine expression in gastric epithelial cells. The Janus kinase/signal transducers and activators of transcription (Jak/Stat) cascade is the inflammatory signaling in various cells. The purpose of the present study is to determine whether H. pylori-induced activation of NF-κB and the expression of interleukin-8 (IL-8) are mediated by the activation of Jak1/Stat3 in gastric epithelial (AGS) cells. Thus, gastric epithelial AGS cells were infected with H. pylori in Korean isolates (HP99) at bacterium/cell ratio of 300:1, and the level of IL-8 in the medium was determined by enzyme-linked immonosorbent assay. Phospho-specific and total forms of Jak1/Stat3 and IκBα were assessed by Western blot analysis, and NF-κB activation was determined by electrophoretic mobility shift assay. The results showed that H. pylori induced the activation of Jak1/Stat3 and IL-8 production, which was inhibited by a Jak/Stat3 specific inhibitor AG490 in AGS cells in a dose-dependent manner. H. pylori-induced activation of NF-κB, determined by phosphorylation of IκBα and NF-κB-DNA binding activity, were inhibited by AG490. In conclusion, Jak1/Stat3 activation may mediate the activation of NF-κB and the expression of IL-8 in H. pylori-infected AGS cells. Inhibition of Jak1/Stat3 may be beneficial for the treatment of H. pylori-induced gastric inflammation, since the activation of NF-κB is inhibited and inflammatory cytokine expression is suppressed. |
format | Online Article Text |
id | pubmed-4397461 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Yonsei University College of Medicine |
record_format | MEDLINE/PubMed |
spelling | pubmed-43974612015-05-01 Jak1/Stat3 Is an Upstream Signaling of NF-κB Activation in Helicobacter pylori-Induced IL-8 Production in Gastric Epithelial AGS Cells Cha, Boram Lim, Joo Weon Kim, Hyeyoung Yonsei Med J Brief Communication Helicobacter pylori (H. pylori) induces the activation of nuclear factor-kB (NF-κB) and cytokine expression in gastric epithelial cells. The Janus kinase/signal transducers and activators of transcription (Jak/Stat) cascade is the inflammatory signaling in various cells. The purpose of the present study is to determine whether H. pylori-induced activation of NF-κB and the expression of interleukin-8 (IL-8) are mediated by the activation of Jak1/Stat3 in gastric epithelial (AGS) cells. Thus, gastric epithelial AGS cells were infected with H. pylori in Korean isolates (HP99) at bacterium/cell ratio of 300:1, and the level of IL-8 in the medium was determined by enzyme-linked immonosorbent assay. Phospho-specific and total forms of Jak1/Stat3 and IκBα were assessed by Western blot analysis, and NF-κB activation was determined by electrophoretic mobility shift assay. The results showed that H. pylori induced the activation of Jak1/Stat3 and IL-8 production, which was inhibited by a Jak/Stat3 specific inhibitor AG490 in AGS cells in a dose-dependent manner. H. pylori-induced activation of NF-κB, determined by phosphorylation of IκBα and NF-κB-DNA binding activity, were inhibited by AG490. In conclusion, Jak1/Stat3 activation may mediate the activation of NF-κB and the expression of IL-8 in H. pylori-infected AGS cells. Inhibition of Jak1/Stat3 may be beneficial for the treatment of H. pylori-induced gastric inflammation, since the activation of NF-κB is inhibited and inflammatory cytokine expression is suppressed. Yonsei University College of Medicine 2015-05-01 2015-04-01 /pmc/articles/PMC4397461/ /pubmed/25837197 http://dx.doi.org/10.3349/ymj.2015.56.3.862 Text en © Copyright: Yonsei University College of Medicine 2015 http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Brief Communication Cha, Boram Lim, Joo Weon Kim, Hyeyoung Jak1/Stat3 Is an Upstream Signaling of NF-κB Activation in Helicobacter pylori-Induced IL-8 Production in Gastric Epithelial AGS Cells |
title | Jak1/Stat3 Is an Upstream Signaling of NF-κB Activation in Helicobacter pylori-Induced IL-8 Production in Gastric Epithelial AGS Cells |
title_full | Jak1/Stat3 Is an Upstream Signaling of NF-κB Activation in Helicobacter pylori-Induced IL-8 Production in Gastric Epithelial AGS Cells |
title_fullStr | Jak1/Stat3 Is an Upstream Signaling of NF-κB Activation in Helicobacter pylori-Induced IL-8 Production in Gastric Epithelial AGS Cells |
title_full_unstemmed | Jak1/Stat3 Is an Upstream Signaling of NF-κB Activation in Helicobacter pylori-Induced IL-8 Production in Gastric Epithelial AGS Cells |
title_short | Jak1/Stat3 Is an Upstream Signaling of NF-κB Activation in Helicobacter pylori-Induced IL-8 Production in Gastric Epithelial AGS Cells |
title_sort | jak1/stat3 is an upstream signaling of nf-κb activation in helicobacter pylori-induced il-8 production in gastric epithelial ags cells |
topic | Brief Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4397461/ https://www.ncbi.nlm.nih.gov/pubmed/25837197 http://dx.doi.org/10.3349/ymj.2015.56.3.862 |
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