scholarly journals Essential Roles of NF-κB and C/EBP in the Regulation of Intercellular Adhesion Molecule-1 after Respiratory Syncytial Virus Infection of Human Respiratory Epithelial Cell Cultures

1998 ◽  
Vol 72 (2) ◽  
pp. 1623-1626 ◽  
Author(s):  
B. A. Chini ◽  
M. A. Fiedler ◽  
L. Milligan ◽  
T. Hopkins ◽  
J. M. Stark
Keyword(s):  
Respiratory Syncytial Virus ◽  
Cell Cultures ◽  
Adhesion Molecule ◽  
Critical Role ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Luciferase Reporter ◽  
Intercellular Adhesion Molecule 1 ◽  
Syncytial Virus ◽  
Respiratory Epithelial

ABSTRACT To determine the molecular mechanism(s) of respiratory syncytial virus (RSV)-induced intercellular adhesion molecule-1 (ICAM-1) upregulation in respiratory epithelial cells (REC; A549 cell cultures), we investigated the roles of the transcription factors NF-κB and C/EBP. Increases in ICAM-1 message required de novo mRNA synthesis. ICAM-1 promoter constructs (luciferase reporter gene) transfected into A549 monolayers demonstrated promoter activation following RSV infection. Activation was abolished by site-specific mutation of the NF-κB (−228) or C/EBP (−239) sites. These data support the critical role of the activation of NF-κB and C/EBP in RSV-induced ICAM-1 expression by REC.

scholarly journals Activation of Intercellular Adhesion Molecule 1 Expression by Helicobacter pylori Is Regulated by NF-κB in Gastric Epithelial Cancer Cells

2000 ◽  
Vol 68 (4) ◽  
pp. 1806-1814 ◽  
Author(s):  
Naoki Mori ◽  
Akihiro Wada ◽  
Toshiya Hirayama ◽  
Thomas P. Parks ◽  
Christian Stratowa ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Luciferase Reporter ◽  
Pyrrolidine Dithiocarbamate ◽  
Mrna Levels ◽  
Intercellular Adhesion Molecule 1 ◽  
H Pylori

ABSTRACT Interactions between leukocytes and epithelial cells may play a key role in Helicobacter pylori-associated gastric mucosal inflammation. This process is mediated by various cell adhesion molecules. The present study examined the molecular mechanisms leading to H. pylori-induced epithelial cell intercellular adhesion molecule-1 (ICAM-1; also called CD54) expression. Coculture of epithelial cells with cytotoxin-associated gene pathogenicity island-positive (cag PAI+) H. pylori strains, but not with a cag PAI−strain or H. pylori culture supernatants, resulted in upregulation of steady-state mRNA levels and cell surface expression of ICAM-1. Coculture with H. pylori induced an increase in luciferase activity in cells which were transfected with a luciferase reporter gene linked to the 5′-flanking region of the ICAM-1 gene.H. pylori activated the ICAM-1 promoter via the NF-κB binding site. An inducible nuclear protein complex bound to the ICAM-1 NF-κB site and was identified as the NF-κB p50–p65 heterodimer.H. pylori induced the degradation of IκB-α, a major cytoplasmic inhibitor of NF-κB, and stimulated the expression of IκB-α mRNA. Pretreatment of epithelial cells with pyrrolidine dithiocarbamate, which blocks NF-κB activation, inhibited H. pylori-induced ICAM-1 expression. THP-1 macrophagic cells, peripheral blood mononuclear cells, and purified neutrophils adhered toH. pylori-infected epithelial cells to a greater extent than to uninfected cells. These results show that H. pyloridirectly induces expression of ICAM-1 on gastric epithelial cells in an NF-κB-dependent manner that may support leukocyte attachment during inflammation.

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