Helicobacter pylori-derived Heat Shock Protein 60 Induce the Decrease in the Proliferation of Peripheral Blood Mononuclear Cells and the Increase in Treg Cell via TGF-? signaling pathway

碩士 === 國立交通大學 === 分子醫學與生物工程研究所 === 98 === Helicobacter pylori can lead to variety of upper gastrointestinal disorders such as chronic gastritis, peptic ulcer disease, gastric mucosa- associated lymphoid tissue (MALT) lymphoma and gastric cancer. Without treatment, H. pylori would become chronic inf...

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Main Authors: Hsu, Wei-Tung, 徐維瞳
Other Authors: Liao, Kuang-Wen
Format: Others
Language:en_US
Published: 2010
Online Access:http://ndltd.ncl.edu.tw/handle/46952476103271516293
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spelling ndltd-TW-098NCTU55380022016-04-25T04:27:51Z http://ndltd.ncl.edu.tw/handle/46952476103271516293 Helicobacter pylori-derived Heat Shock Protein 60 Induce the Decrease in the Proliferation of Peripheral Blood Mononuclear Cells and the Increase in Treg Cell via TGF-? signaling pathway 幽門螺旋桿菌之熱休克蛋白60可藉由乙型轉化生長因子訊息傳遞路徑抑制週邊血液單核球細胞之增生 Hsu, Wei-Tung 徐維瞳 碩士 國立交通大學 分子醫學與生物工程研究所 98 Helicobacter pylori can lead to variety of upper gastrointestinal disorders such as chronic gastritis, peptic ulcer disease, gastric mucosa- associated lymphoid tissue (MALT) lymphoma and gastric cancer. Without treatment, H. pylori would become chronic infection in almost all of those patients. Although the virulent factors of H. pylori such as CagA, VacA have been demonstrated to play roles in H.pylori colonization and persistent infection, not all the strains isolated form clinic carry those virulent factors. Thus, the universal mechanism of the chronic infection for all stains of this pathogen still is unclear. Maybe, certain factor(s) is involved in this immunosuppressive mechanism, which is necessary to be explored. Interestedly, researchers found that Heat shock protein 60 (Hsp60) seems to be related to the regulation of immune responds in chronic infection disease. Literatures indicated that Hsp60s in C. albicans or M. tuberculosis can induce persistent colonization in the murine experimental model. Therefore, the Hsp60 of H. pylori was considered that it may be an immunosuppressive factor. In this study, we investigated the role of H. pylori Hsp60 (HpHsp60) in immunosuppression. The results showed that the treatment with HpHsp60 to human peripheral blood mononuclear cells (PBMCs) decreased the proliferation rate, changed the cytokine secretion profile, and induce cell cycle arrest. Intracellular FoxP3 staining showed the regulatory T cells were increased after HpHsp60 treatment. Furthermore a TGF-? signaling pathway is shown to be involved in the generation of HpHsp60-induced Treg cells. Taken together, the treatment of HpHsp60 might generate the regulatory T cells and thus help H. pylori to escape from the attacks evoked by human immune system. Liao, Kuang-Wen 廖光文 2010 學位論文 ; thesis 61 en_US
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language en_US
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description 碩士 === 國立交通大學 === 分子醫學與生物工程研究所 === 98 === Helicobacter pylori can lead to variety of upper gastrointestinal disorders such as chronic gastritis, peptic ulcer disease, gastric mucosa- associated lymphoid tissue (MALT) lymphoma and gastric cancer. Without treatment, H. pylori would become chronic infection in almost all of those patients. Although the virulent factors of H. pylori such as CagA, VacA have been demonstrated to play roles in H.pylori colonization and persistent infection, not all the strains isolated form clinic carry those virulent factors. Thus, the universal mechanism of the chronic infection for all stains of this pathogen still is unclear. Maybe, certain factor(s) is involved in this immunosuppressive mechanism, which is necessary to be explored. Interestedly, researchers found that Heat shock protein 60 (Hsp60) seems to be related to the regulation of immune responds in chronic infection disease. Literatures indicated that Hsp60s in C. albicans or M. tuberculosis can induce persistent colonization in the murine experimental model. Therefore, the Hsp60 of H. pylori was considered that it may be an immunosuppressive factor. In this study, we investigated the role of H. pylori Hsp60 (HpHsp60) in immunosuppression. The results showed that the treatment with HpHsp60 to human peripheral blood mononuclear cells (PBMCs) decreased the proliferation rate, changed the cytokine secretion profile, and induce cell cycle arrest. Intracellular FoxP3 staining showed the regulatory T cells were increased after HpHsp60 treatment. Furthermore a TGF-? signaling pathway is shown to be involved in the generation of HpHsp60-induced Treg cells. Taken together, the treatment of HpHsp60 might generate the regulatory T cells and thus help H. pylori to escape from the attacks evoked by human immune system.
author2 Liao, Kuang-Wen
author_facet Liao, Kuang-Wen
Hsu, Wei-Tung
徐維瞳
author Hsu, Wei-Tung
徐維瞳
spellingShingle Hsu, Wei-Tung
徐維瞳
Helicobacter pylori-derived Heat Shock Protein 60 Induce the Decrease in the Proliferation of Peripheral Blood Mononuclear Cells and the Increase in Treg Cell via TGF-? signaling pathway
author_sort Hsu, Wei-Tung
title Helicobacter pylori-derived Heat Shock Protein 60 Induce the Decrease in the Proliferation of Peripheral Blood Mononuclear Cells and the Increase in Treg Cell via TGF-? signaling pathway
title_short Helicobacter pylori-derived Heat Shock Protein 60 Induce the Decrease in the Proliferation of Peripheral Blood Mononuclear Cells and the Increase in Treg Cell via TGF-? signaling pathway
title_full Helicobacter pylori-derived Heat Shock Protein 60 Induce the Decrease in the Proliferation of Peripheral Blood Mononuclear Cells and the Increase in Treg Cell via TGF-? signaling pathway
title_fullStr Helicobacter pylori-derived Heat Shock Protein 60 Induce the Decrease in the Proliferation of Peripheral Blood Mononuclear Cells and the Increase in Treg Cell via TGF-? signaling pathway
title_full_unstemmed Helicobacter pylori-derived Heat Shock Protein 60 Induce the Decrease in the Proliferation of Peripheral Blood Mononuclear Cells and the Increase in Treg Cell via TGF-? signaling pathway
title_sort helicobacter pylori-derived heat shock protein 60 induce the decrease in the proliferation of peripheral blood mononuclear cells and the increase in treg cell via tgf-? signaling pathway
publishDate 2010
url http://ndltd.ncl.edu.tw/handle/46952476103271516293
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