Cited 4 times in

Vibrio vulnificus IlpA induces MAPK-mediated cytokine production via TLR1/2 activation in THP-1 cells, a human monocytic cell line

Authors
 Na Yeon Lee ; Hye-Yeon Lee ; Soon-Jung Park ; Seung Hyun Han ; Kyu-Ho Lee 
Citation
 Molecular Immunology, Vol.49(1-2) : 143~154, 2011 
Journal Title
 Molecular Immunology 
ISSN
 0161-5890 
Issue Date
2011
Abstract
Vibrio vulnificus is a pathogenic bacterium causing primary septicemia, which is followed by a classical septic shock pathway including an overwhelming inflammatory cytokine response. V. vulnificus IlpA is a potent immunogenic lipoprotein that triggers cytokine production in human monocytes by activating the toll-like receptor 2 (TLR2). In this study, we further defined the IlpA signaling pathways involved in cytokine production in the human monocytic cell line, THP-1. TLR2 was involved in cytokine production by complexing with TLR1, but not with TLR6. MyD88 was necessary for IlpA-induced cytokine expression through TLR1/TLR2. Three mitogen activated protein kinases (MAPK), p38, ERK1/2, and JNK, were activated in THP-1 cells stimulated with recombinant IlpA (rIlpA). Selective inhibition of each MAPK resulted in significant decrease of rIlpA-induced cytokine production. Especially, functional TLR2 was necessary for IlpA-induced activation of p38 and JNK. IlpA augmented the DNA-binding activity of nuclear factor-kappaB (NF-κB) and activator protein-1 (AP-1) transcriptional factors to their recognition sites in THP-1 cells. These results suggest that serial activation of TLR1/TLR2, MyD88, the three MAPKs, and NF-κB/AP-1 comprises the signaling pathway responsible for proinflammatory cytokine production by V. vulnificus IlpA.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/94660
DOI
10.1016/j.molimm.2011.08.001
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Dept. of Environmental Medical Biology
Yonsei Authors
사서에게 알리기
  feedback
Link
 http://www.sciencedirect.com/science/article/pii/S0161589011006924
Export
RIS (EndNote)
XLS (Excel)
XML

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse