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
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作者:
Chini, BA
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机构:Childrens Hosp, Med Ctr, Div Pulm Med, Cincinnati, OH 45229 USA
Chini, BA
Fiedler, MA
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机构:Childrens Hosp, Med Ctr, Div Pulm Med, Cincinnati, OH 45229 USA
Fiedler, MA
Milligan, L
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机构:Childrens Hosp, Med Ctr, Div Pulm Med, Cincinnati, OH 45229 USA
Milligan, L
Hopkins, T
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机构:Childrens Hosp, Med Ctr, Div Pulm Med, Cincinnati, OH 45229 USA
Hopkins, T
Stark, JM
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机构:Childrens Hosp, Med Ctr, Div Pulm Med, Cincinnati, OH 45229 USA
Stark, JM
机构:
[1] Childrens Hosp, Med Ctr, Div Pulm Med, Cincinnati, OH 45229 USA
[2] Childrens Hosp, Div Pulm Med, Pittsburgh, PA 15213 USA
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), se investigated the roles of the transcription factors NF-kappa B 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-kappa B (-228) or C/EBP (-239) sites. These data support the critical role of the activation of NF-kappa B and C/EBP in RSV-induced ICAM-1 expression by REC.