Reducing agents inhibit rhinovirus-induced up-regulation of the rhinovirus receptor intercellular adhesion molecule-1 (ICAM-1) in respiratory epithelial cells
Reducing agents inhibit rhinovirus-induced up-regulation of the rhinovirus receptor intercellular adhesion molecule-1 (ICAM-1) in respiratory epithelial cells
Rhinoviruses are the major cause of common colds and of asthma exacerbations. Intercellular adhesion molecule-1 (ICAM-1) has a central role in airway inflammation and is the receptor for 90% of rhinoviruses. Rhinovirus infection of airway epithelium induces ICAM-1. Because redox state is directly implicated in inflammatory responses via molecular signaling mechanisms, here we studied the effects of reducing agents on rhinovirus-induced ICAM-1 expression, mRNA up-regulation, promoter activation, and nuclear factor activation. To investigate the effects of rhinovirus infection on the intracellular redox balance, we also studied whether rhinovirus infection triggers the production of reactive oxygen species. We found that reduced (GSH) but not oxidized (GSSG) glutathione (1-100 mM) inhibited in a dose-dependent manner rhinovirus-induced ICAM-1 up-regulation and mRNA induction in primary bronchial and A549 respiratory epithelial cells. GSH but not GSSG also inhibited rhinovirus-induced ICAM-1 promoter activation and rhinovirus-induced NF-kB activation. In parallel, we found that rhinovirus infection induced a rapid increase of intracellular superoxide anion that was maximal at the time of NF-kB activation. This oxidant generation was completely inhibited by GSH. We conclude that redox-mediated intracellular pathways represent an important target for the therapeutic control of rhinovirus-induced diseases.
asthma, rhinitis, oxidants, nuclear factor kB
1934-1936
Papi, Alberto
8447eef8-34fd-482e-8e91-f8231acd05f7
Papadopoulos, Nikolaos
53d807da-b3b5-45d8-9810-a7d7c343fadc
Stanciu, Luminita A.
92eb55fa-d20e-4d3a-aa71-207eaf6bceca
Bellettato, Cinzia M.
e1742263-a3d5-4fbf-b127-0731599db7fb
Pinamonti, Silvano
f785f499-57e0-4411-afbb-ba59f88495cd
Degitz, Klaus
5b169fb4-20f2-4e71-b506-1fc5acdfc7e2
Holgate, Stephen T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Johnston, Sebastian L.
90e0ef79-cfde-40e0-b301-90d3063ee036
2002
Papi, Alberto
8447eef8-34fd-482e-8e91-f8231acd05f7
Papadopoulos, Nikolaos
53d807da-b3b5-45d8-9810-a7d7c343fadc
Stanciu, Luminita A.
92eb55fa-d20e-4d3a-aa71-207eaf6bceca
Bellettato, Cinzia M.
e1742263-a3d5-4fbf-b127-0731599db7fb
Pinamonti, Silvano
f785f499-57e0-4411-afbb-ba59f88495cd
Degitz, Klaus
5b169fb4-20f2-4e71-b506-1fc5acdfc7e2
Holgate, Stephen T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Johnston, Sebastian L.
90e0ef79-cfde-40e0-b301-90d3063ee036
Papi, Alberto, Papadopoulos, Nikolaos, Stanciu, Luminita A., Bellettato, Cinzia M., Pinamonti, Silvano, Degitz, Klaus, Holgate, Stephen T. and Johnston, Sebastian L.
(2002)
Reducing agents inhibit rhinovirus-induced up-regulation of the rhinovirus receptor intercellular adhesion molecule-1 (ICAM-1) in respiratory epithelial cells.
FASEB Journal, 16 (14), .
(doi:10.1096/fj.02-0118fje).
Abstract
Rhinoviruses are the major cause of common colds and of asthma exacerbations. Intercellular adhesion molecule-1 (ICAM-1) has a central role in airway inflammation and is the receptor for 90% of rhinoviruses. Rhinovirus infection of airway epithelium induces ICAM-1. Because redox state is directly implicated in inflammatory responses via molecular signaling mechanisms, here we studied the effects of reducing agents on rhinovirus-induced ICAM-1 expression, mRNA up-regulation, promoter activation, and nuclear factor activation. To investigate the effects of rhinovirus infection on the intracellular redox balance, we also studied whether rhinovirus infection triggers the production of reactive oxygen species. We found that reduced (GSH) but not oxidized (GSSG) glutathione (1-100 mM) inhibited in a dose-dependent manner rhinovirus-induced ICAM-1 up-regulation and mRNA induction in primary bronchial and A549 respiratory epithelial cells. GSH but not GSSG also inhibited rhinovirus-induced ICAM-1 promoter activation and rhinovirus-induced NF-kB activation. In parallel, we found that rhinovirus infection induced a rapid increase of intracellular superoxide anion that was maximal at the time of NF-kB activation. This oxidant generation was completely inhibited by GSH. We conclude that redox-mediated intracellular pathways represent an important target for the therapeutic control of rhinovirus-induced diseases.
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Published date: 2002
Keywords:
asthma, rhinitis, oxidants, nuclear factor kB
Organisations:
Infection Inflammation & Immunity
Identifiers
Local EPrints ID: 27311
URI: http://eprints.soton.ac.uk/id/eprint/27311
ISSN: 0892-6638
PURE UUID: db53e793-9e76-4a09-98b2-c494bfaddf31
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Date deposited: 26 Apr 2006
Last modified: 15 Mar 2024 07:17
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Contributors
Author:
Alberto Papi
Author:
Nikolaos Papadopoulos
Author:
Luminita A. Stanciu
Author:
Cinzia M. Bellettato
Author:
Silvano Pinamonti
Author:
Klaus Degitz
Author:
Sebastian L. Johnston
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