Cargando…
Helicobacter pylori Outer Membrane Protein 18 (Hp1125) Is Involved in Persistent Colonization by Evading Interferon-γ Signaling
Outer membrane proteins (OMPs) can induce an immune response. Omp18 (HP1125) of H. pylori is a powerful antigen that can induce significant interferon-γ (IFN-γ) levels. Previous studies have suggested that IFN-γ plays an important role in H. pylori clearance. However, H. pylori has multiple mechanis...
Autores principales: | , , , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2015
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4402576/ https://www.ncbi.nlm.nih.gov/pubmed/25945338 http://dx.doi.org/10.1155/2015/571280 |
_version_ | 1782367280327294976 |
---|---|
author | Shan, Yuqun Lu, Xingxiao Han, Yingnan Li, Xinpeng Wang, Xiao Shao, Chunhong Wang, Lixiang Liu, Zhifang Tang, Wei Sun, Yundong Jia, Jihui |
author_facet | Shan, Yuqun Lu, Xingxiao Han, Yingnan Li, Xinpeng Wang, Xiao Shao, Chunhong Wang, Lixiang Liu, Zhifang Tang, Wei Sun, Yundong Jia, Jihui |
author_sort | Shan, Yuqun |
collection | PubMed |
description | Outer membrane proteins (OMPs) can induce an immune response. Omp18 (HP1125) of H. pylori is a powerful antigen that can induce significant interferon-γ (IFN-γ) levels. Previous studies have suggested that IFN-γ plays an important role in H. pylori clearance. However, H. pylori has multiple mechanisms to avoid host immune surveillance for persistent colonization. We generated an omp18 mutant (H. pylori 26695 and H. pylori SS1) strain to examine whether Omp18 interacts with IFN-γ and is involved in H. pylori colonization. qRT-PCR revealed that IFN-γ induced Omp18 expression. qRT-PCR and western blot analysis revealed reduced expressions of virulence factors CagA and NapA in H. pylori 26695 with IFN-γ treatment, but they were induced in the Δomp18 strain. In C57BL/6 mice infected with H. pylori SS1 and the Δomp18 strain, the Δomp18 strain conferred defective colonization and activated a stronger inflammatory response. Signal transducer phosphorylation and transcription 1 (STAT1) activator was downregulated by the wild-type strain but not the Δomp18 strain in IFN-γ-treated macrophages. Furthermore, Δomp18 strain survival rates were poor in macrophages compared to the wild-type strain. We concluded that H. pylori Omp18 has an important function influencing IFN-γ-mediated immune response to participate in persistent colonization. |
format | Online Article Text |
id | pubmed-4402576 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-44025762015-05-05 Helicobacter pylori Outer Membrane Protein 18 (Hp1125) Is Involved in Persistent Colonization by Evading Interferon-γ Signaling Shan, Yuqun Lu, Xingxiao Han, Yingnan Li, Xinpeng Wang, Xiao Shao, Chunhong Wang, Lixiang Liu, Zhifang Tang, Wei Sun, Yundong Jia, Jihui Biomed Res Int Research Article Outer membrane proteins (OMPs) can induce an immune response. Omp18 (HP1125) of H. pylori is a powerful antigen that can induce significant interferon-γ (IFN-γ) levels. Previous studies have suggested that IFN-γ plays an important role in H. pylori clearance. However, H. pylori has multiple mechanisms to avoid host immune surveillance for persistent colonization. We generated an omp18 mutant (H. pylori 26695 and H. pylori SS1) strain to examine whether Omp18 interacts with IFN-γ and is involved in H. pylori colonization. qRT-PCR revealed that IFN-γ induced Omp18 expression. qRT-PCR and western blot analysis revealed reduced expressions of virulence factors CagA and NapA in H. pylori 26695 with IFN-γ treatment, but they were induced in the Δomp18 strain. In C57BL/6 mice infected with H. pylori SS1 and the Δomp18 strain, the Δomp18 strain conferred defective colonization and activated a stronger inflammatory response. Signal transducer phosphorylation and transcription 1 (STAT1) activator was downregulated by the wild-type strain but not the Δomp18 strain in IFN-γ-treated macrophages. Furthermore, Δomp18 strain survival rates were poor in macrophages compared to the wild-type strain. We concluded that H. pylori Omp18 has an important function influencing IFN-γ-mediated immune response to participate in persistent colonization. Hindawi Publishing Corporation 2015 2015-04-06 /pmc/articles/PMC4402576/ /pubmed/25945338 http://dx.doi.org/10.1155/2015/571280 Text en Copyright © 2015 Yuqun Shan et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Shan, Yuqun Lu, Xingxiao Han, Yingnan Li, Xinpeng Wang, Xiao Shao, Chunhong Wang, Lixiang Liu, Zhifang Tang, Wei Sun, Yundong Jia, Jihui Helicobacter pylori Outer Membrane Protein 18 (Hp1125) Is Involved in Persistent Colonization by Evading Interferon-γ Signaling |
title |
Helicobacter pylori Outer Membrane Protein 18 (Hp1125) Is Involved in Persistent Colonization by Evading Interferon-γ Signaling |
title_full |
Helicobacter pylori Outer Membrane Protein 18 (Hp1125) Is Involved in Persistent Colonization by Evading Interferon-γ Signaling |
title_fullStr |
Helicobacter pylori Outer Membrane Protein 18 (Hp1125) Is Involved in Persistent Colonization by Evading Interferon-γ Signaling |
title_full_unstemmed |
Helicobacter pylori Outer Membrane Protein 18 (Hp1125) Is Involved in Persistent Colonization by Evading Interferon-γ Signaling |
title_short |
Helicobacter pylori Outer Membrane Protein 18 (Hp1125) Is Involved in Persistent Colonization by Evading Interferon-γ Signaling |
title_sort | helicobacter pylori outer membrane protein 18 (hp1125) is involved in persistent colonization by evading interferon-γ signaling |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4402576/ https://www.ncbi.nlm.nih.gov/pubmed/25945338 http://dx.doi.org/10.1155/2015/571280 |
work_keys_str_mv | AT shanyuqun helicobacterpylorioutermembraneprotein18hp1125isinvolvedinpersistentcolonizationbyevadinginterferongsignaling AT luxingxiao helicobacterpylorioutermembraneprotein18hp1125isinvolvedinpersistentcolonizationbyevadinginterferongsignaling AT hanyingnan helicobacterpylorioutermembraneprotein18hp1125isinvolvedinpersistentcolonizationbyevadinginterferongsignaling AT lixinpeng helicobacterpylorioutermembraneprotein18hp1125isinvolvedinpersistentcolonizationbyevadinginterferongsignaling AT wangxiao helicobacterpylorioutermembraneprotein18hp1125isinvolvedinpersistentcolonizationbyevadinginterferongsignaling AT shaochunhong helicobacterpylorioutermembraneprotein18hp1125isinvolvedinpersistentcolonizationbyevadinginterferongsignaling AT wanglixiang helicobacterpylorioutermembraneprotein18hp1125isinvolvedinpersistentcolonizationbyevadinginterferongsignaling AT liuzhifang helicobacterpylorioutermembraneprotein18hp1125isinvolvedinpersistentcolonizationbyevadinginterferongsignaling AT tangwei helicobacterpylorioutermembraneprotein18hp1125isinvolvedinpersistentcolonizationbyevadinginterferongsignaling AT sunyundong helicobacterpylorioutermembraneprotein18hp1125isinvolvedinpersistentcolonizationbyevadinginterferongsignaling AT jiajihui helicobacterpylorioutermembraneprotein18hp1125isinvolvedinpersistentcolonizationbyevadinginterferongsignaling |