PMID- 25041690
OWN - NLM
STAT- MEDLINE
DCOM- 20150910
LR  - 20211203
IS  - 1440-1746 (Electronic)
IS  - 0815-9319 (Linking)
VI  - 30
IP  - 1
DP  - 2015 Jan
TI  - Helicobacter pylori vacuolating cytotoxin induces apoptosis via activation of 
      endoplasmic reticulum stress in dendritic cells.
PG  - 99-108
LID - 10.1111/jgh.12663 [doi]
AB  - BACKGROUND AND AIM: Dendritic cells (DCs) are observed on the Helicobacter 
      pylori-infected gastric mucosa. DCs generally play an important role in the 
      regulation of inflammation. Although stimulation of gastric epithelial cells with 
      H. pylori vacuolating cytotoxin (VacA) has been reported to induce apoptosis and 
      endoplasmic reticulum (ER) stress, the effects of VacA on the DC apoptotic 
      response have not been well elucidated. This study was conducted to investigate 
      the role of H. pylori VacA on the apoptotic process and ER stress in DCs. 
      METHODS: Murine and human DCs were generated from specific pathogen-free C57BL/6 
      mice and human peripheral blood mononuclear cells, respectively. DCs were 
      incubated with purified VacA, after which Bax activation, cytochrome c release, 
      and DNA fragmentation for apoptosis were measured by fluorescent microscopy, 
      immunoblot, and ELISA. ER stress-related molecules such as GRP78 and CHOP were 
      analyzed by immunoblot. RESULTS: Treatment of DCs with purified H. pylori VacA 
      resulted in the induction of apoptosis. DC stimulation with VacA led to the 
      translocation of cytoplasmic Bax to mitochondria and cytochrome c release from 
      mitochondria. H. pylori VacA induced signals for ER stress early during the 
      stimulation process in DCs. Furthermore, suppression of ER stress resulted in a 
      significant inhibition of the VacA-induced apoptosis in DCs. CONCLUSION: These 
      results suggest that ER stress is critical for regulation of DC apoptotic process 
      in response to VacA stimulation.
CI  - (c) 2014 Journal of Gastroenterology and Hepatology Foundation and Wiley Publishing 
      Asia Pty Ltd.
FAU - Kim, Jung Mogg
AU  - Kim JM
AD  - Department of Microbiology, Hanyang University College of Medicine, Seoul, Korea.
FAU - Kim, Joo Sung
AU  - Kim JS
FAU - Kim, Nayoung
AU  - Kim N
FAU - Ko, Su Hyuk
AU  - Ko SH
FAU - Jeon, Jong Ik
AU  - Jeon JI
FAU - Kim, Young-Jeon
AU  - Kim YJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Australia
TA  - J Gastroenterol Hepatol
JT  - Journal of gastroenterology and hepatology
JID - 8607909
RN  - 0 (Bacterial Proteins)
RN  - 0 (DDIT3 protein, human)
RN  - 0 (Endoplasmic Reticulum Chaperone BiP)
RN  - 0 (HSPA5 protein, human)
RN  - 0 (Heat-Shock Proteins)
RN  - 0 (Hspa5 protein, mouse)
RN  - 0 (VacA protein, Helicobacter pylori)
RN  - 147336-12-7 (Transcription Factor CHOP)
SB  - IM
MH  - Animals
MH  - Apoptosis/*genetics
MH  - Bacterial Proteins/*physiology
MH  - Dendritic Cells/*pathology/physiology
MH  - Endoplasmic Reticulum Chaperone BiP
MH  - Endoplasmic Reticulum Stress/*genetics
MH  - Gastric Mucosa/cytology
MH  - Heat-Shock Proteins/metabolism
MH  - *Helicobacter pylori
MH  - Humans
MH  - Mice, Inbred C57BL
MH  - Transcription Factor CHOP/metabolism
OTO - NOTNLM
OT  - ER stress
OT  - H. pylori vacuolating cytotoxin
OT  - apoptosis
OT  - dendritic cells
EDAT- 2014/07/22 06:00
MHDA- 2015/09/12 06:00
CRDT- 2014/07/22 06:00
PHST- 2014/05/22 00:00 [accepted]
PHST- 2014/07/22 06:00 [entrez]
PHST- 2014/07/22 06:00 [pubmed]
PHST- 2015/09/12 06:00 [medline]
AID - 10.1111/jgh.12663 [doi]
PST - ppublish
SO  - J Gastroenterol Hepatol. 2015 Jan;30(1):99-108. doi: 10.1111/jgh.12663.