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Vibrio vulnificus-induced cell death of human mononuclear cells requires ROS-dependent activation of p38 and ERK 1/2 MAPKs

Authors
 Woo Hyang Kim  ;  Sung Young Goo  ;  Kyu-Ho Lee  ;  Soon-Jung Park 
Citation
 IMMUNOLOGICAL INVESTIGATIONS, Vol.38(1) : 31-48, 2009 
Journal Title
IMMUNOLOGICAL INVESTIGATIONS
ISSN
 0882-0139 
Issue Date
2009
MeSH
Cell Death/drug effects ; Cell Death/immunology ; Cells, Cultured ; Enzyme Activation/drug effects ; Extracellular Signal-Regulated MAP Kinases/immunology ; Extracellular Signal-Regulated MAP Kinases/metabolism* ; Humans ; Leukocytes, Mononuclear/immunology ; Leukocytes, Mononuclear/metabolism* ; Leukocytes, Mononuclear/microbiology ; Leukocytes, Mononuclear/pathology ; Nitric Oxide/antagonists & inhibitors ; Nitric Oxide/immunology ; Nitric Oxide Synthase Type II/immunology ; Nitric Oxide Synthase Type II/metabolism ; Onium Compounds/pharmacology ; Oxidative Phosphorylation/drug effects ; Reactive Oxygen Species/antagonists & inhibitors ; Reactive Oxygen Species/immunology* ; Signal Transduction/drug effects ; Vibrio Infections/enzymology ; Vibrio Infections/immunology* ; Vibrio vulnificus/immunology* ; Vibrio vulnificus/pathogenicity ; p38 Mitogen-Activated Protein Kinases/immunology ; p38 Mitogen-Activated Protein Kinases/metabolism*
Keywords
Vibrio vulnificus ; Reactive oxygen species ; Mitogen-activated protein kinases ; Human peripheral blood mononuclear cells
Abstract
Vibrio vulnificus is a Gram-negative bacterium that multiplies rapidly in host tissue and causes extensive tissue damage. Human peripheral blood mononuclear cells (PBMC) were shown to be readily killed by exposure to live V. vulnificus. V. vulnificus induced production of intracellular reactive oxygen species (ROS) and nitric oxide (NO) in PBMC. Pretreatment of PBMC with diphenyleneiodonium chloride (DPI) abolished ROS generation upon exposure to V. vulnificus and decreased the bacterial ability to cause cell death. In contrast, pretreatment of these cells with inhibitors of inducible nitric oxide synthase (iNOS) blocked V. vunificus-induced NO production, but did not significantly alter cell death by V. vulnificus. V. vulnificus also triggered phosphorylation of mitogen-activated protein kinases (MAPKs), including p38 and ERK1/2 in PBMC. Inactivation of these MAPKs by selective inhibitors caused a reduction both in ROS generation and cell death induced by V. vulnificus. It was further shown that an inhibitor of ROS generation (DPI) blocked V. vulnificus-induced phosphorylation of p38 and ERK1/2 MAPK. This study demonstrates that V. vulnificus induces death of PBMC via ROS-dependent activation of p38 MAPK and ERK1/2 MAPK.
Full Text
http://informahealthcare.com/doi/abs/10.1080/08820130802500583
DOI
10.1080/08820130802500583
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Tropica Medicine (열대의학교실) > 1. Journal Papers
Yonsei Authors
Kim, Woo Hyang(김우향)
Park, Soon Jung(박순정) ORCID logo https://orcid.org/0000-0002-0423-1944
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/103623
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