DC 欄位 | 值 | 語言 |
dc.contributor.author | 許秉寧 | zh-TW |
dc.creator | 許秉寧 | zh_TW |
dc.date | 2003 | zh_TW |
dc.date.accessioned | 2018-07-09T01:47:34Z | - |
dc.date.available | 2018-07-09T01:47:34Z | - |
dc.date.issued | 2003 | - |
dc.identifier | 912320B002193 | zh_TW |
dc.identifier.uri | http://ntur.lib.ntu.edu.tw//handle/246246/25361 | - |
dc.description.abstract | Helicobacter pylori ( H. pylori) causes a common chronic infection of humans
that causes gastritis and peptic ulcer diseases. The enhanced gastric epithelial cell
apoptosis observed during infection with H. pylori has been suggested to be of
significance in the pathogenesis of gastritis. In addition to direct triggering cell
apoptosis by H. pylori cytotoxins, in our preliminary study, we demonstrated that H.
pylori could modulate intracellular death signal transduction regulatory mechanisms
and confer sensitivity to TNF-related apoptosis inducing ligand (TRAIL) -mediated
apoptosis in gastric epithelial cells. TRAIL, a new member of TNF superfamily
molecule, induces apoptosis in transformed cell lines of diverse origin but not in most
primary cells, indicating that the apoptosis induced by TRAIL is under regulation.
The gastric epithelial cell lines, AGS and KATO III, which were resistant to
TRAIL-induced cell death in vitro; however, when both AGS and KATO III cells
exposed to H. pylori, they exhibited significant apoptosis to TRAIL. The effect of
induction of TRAIL apoptosis by H. pylori is only observed when it is in the presence
of live H. pylori but not heat-killed bacteria. Moreover, the H. pylori induced
enhancement of TRAIL mediated apoptosis in gastric epithelial cells could be
specifically blocked by Caspase-3 and Caspase-8 inhibitors, indicating that the
alteration of TRAIL sensitivity by H. pylori is via modulation of intracellular TRAIL
death signal transduction regulation. Thus, in addition to direct trigger apoptosis in
gastric epithelial cells, H. pylori can induce sensitivity to TRAIL-mediated apoptosis by altering intracellular signal transduction regulation in gastric epithelial cells. In this
project, we attempt to further investigate the possible molecular mechanisms of
TRAIL induced death signals modulated by Helicobacter as well as the pathogenesis
of gastric mucosa damage induced by H. pylori infection in an in vitro co-culture
system. We were able to demonstrated that the induction of TRAIL sensitivity by H.
pylori is independent of expression of H. pylori virulent factors Vac A and Cag A; and
is dependent on viable bacteria and direct contact with cells. H. pylori induced
sensitivity to TRAIL-mediated apoptosis in gastric epithelial cells is dependent on
activation of caspase-8 downstream pathway to convey the death signal to
mitochondria, leading to activation of mitochondrial pathway and breaking the
apoptosis resistance. This study will elucidate the mechanism of apoptosis signal
transduction modulation after interaction with H. pylori. | en |
dc.format | application/pdf | zh_TW |
dc.format.extent | 92155 bytes | - |
dc.format.mimetype | application/pdf | - |
dc.language | zh-TW | zh_TW |
dc.language.iso | zh_TW | - |
dc.publisher | 臺北市:國立臺灣大學醫學院免疫學研究所 | zh_TW |
dc.rights | 國立臺灣大學醫學院免疫學研究所 | zh_TW |
dc.subject | Helicobacter pylori | en |
dc.subject | TRAIL | en |
dc.subject | apoptosis | en |
dc.subject | human gastric epithelial cells | en |
dc.subject | mitochondria | en |
dc.subject.classification | [SDGs]SDG3 | - |
dc.title | 胃幽門螺旋桿菌引起TRAIL所誘發之細胞凋亡訊息傳導的調節機轉(1/2) | zh_TW |
dc.title | Mechanisms of Helicobacter induced modulation
of TRAIL death signal transduction(1/2) | en |
dc.type | journal article | en |
dc.identifier.uri.fulltext | http://ntur.lib.ntu.edu.tw/bitstream/246246/25361/1/912320B002193.pdf | - |
dc.coverage | 計畫年度:91;起迄日期:2002-08-01/2003-07-31 | zh_TW |
item.fulltext | with fulltext | - |
item.languageiso639-1 | zh_TW | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.cerifentitytype | Publications | - |
item.openairetype | journal article | - |
item.grantfulltext | open | - |
顯示於: | 免疫學研究所
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