High-dose hydrocortisone reduces expression of the pro-inflammatory chemokines CXCL8 and CXCL10 in SARS coronavirus-infected intestinal cells.
Identifieur interne : 004814 ( Main/Exploration ); précédent : 004813; suivant : 004815High-dose hydrocortisone reduces expression of the pro-inflammatory chemokines CXCL8 and CXCL10 in SARS coronavirus-infected intestinal cells.
Auteurs : Jindrich Cinatl [Allemagne] ; Martin Michaelis ; Birgit Morgenstern ; Hans Wilhelm DoerrSource :
- International journal of molecular medicine [ 1107-3756 ] ; 2005.
Descripteurs français
- KwdFr :
- ADN (métabolisme), Animaux, Anti-inflammatoires (pharmacologie), Antimétabolites (pharmacologie), Cellules Vero, Chimiokine CXCL10, Chimiokines (métabolisme), Chimiokines CXC (biosynthèse), Facteurs temps, Hydrocortisone (pharmacologie), Inflammation, Interleukine-8 (biosynthèse), Intestins (cytologie), Liaison aux protéines, Lignée cellulaire tumorale, RT-PCR, Ribavirine (pharmacologie), Régulation de l'expression des gènes tumoraux, Régulation positive, Syndrome respiratoire aigu sévère (métabolisme), Test ELISA, Tumeurs du côlon (métabolisme), Tumeurs du côlon (virologie), Virus du SRAS (métabolisme).
- MESH :
- biosynthèse : Chimiokines CXC, Interleukine-8.
- cytologie : Intestins.
- métabolisme : ADN, Chimiokines, Syndrome respiratoire aigu sévère, Tumeurs du côlon, Virus du SRAS.
- pharmacologie : Anti-inflammatoires, Antimétabolites, Hydrocortisone, Ribavirine.
- virologie : Tumeurs du côlon.
- Animaux, Cellules Vero, Chimiokine CXCL10, Facteurs temps, Inflammation, Liaison aux protéines, Lignée cellulaire tumorale, RT-PCR, Régulation de l'expression des gènes tumoraux, Régulation positive, Test ELISA.
English descriptors
- KwdEn :
- Animals, Anti-Inflammatory Agents (pharmacology), Antimetabolites (pharmacology), Cell Line, Tumor, Chemokine CXCL10, Chemokines (metabolism), Chemokines, CXC (biosynthesis), Chlorocebus aethiops, Colonic Neoplasms (metabolism), Colonic Neoplasms (virology), DNA (metabolism), Enzyme-Linked Immunosorbent Assay, Gene Expression Regulation, Neoplastic, Hydrocortisone (pharmacology), Inflammation, Interleukin-8 (biosynthesis), Intestines (cytology), Protein Binding, Reverse Transcriptase Polymerase Chain Reaction, Ribavirin (pharmacology), SARS Virus (metabolism), Severe Acute Respiratory Syndrome (metabolism), Time Factors, Up-Regulation, Vero Cells.
- MESH :
- chemical , biosynthesis : Chemokines, CXC, Interleukin-8.
- chemical , metabolism : Chemokines, DNA.
- chemical , pharmacology : Anti-Inflammatory Agents, Antimetabolites, Hydrocortisone, Ribavirin.
- cytology : Intestines.
- metabolism : Colonic Neoplasms, SARS Virus, Severe Acute Respiratory Syndrome.
- virology : Colonic Neoplasms.
- Animals, Cell Line, Tumor, Chemokine CXCL10, Chlorocebus aethiops, Enzyme-Linked Immunosorbent Assay, Gene Expression Regulation, Neoplastic, Inflammation, Protein Binding, Reverse Transcriptase Polymerase Chain Reaction, Time Factors, Up-Regulation, Vero Cells.
Abstract
Clinical observations and our high-density oligonucleotide microarray results demonstrated increased expression of proinflammatory chemokines after SARS-CoV infection. Here, we investigated the influence of SARS-CoV infection on CXCL8 (interleukin 8) and CXCL10 (interferon-gamma-inducible protein 10) in human intestinal epithelial (Caco2) cells. RT-PCR and ELISA showed time-dependent up-regulation of both chemokines after SARS-CoV infection. Electric mobility shift assay revealed increased DNA binding activity of the cellular transcription factors activator protein 1 (AP-1) and nuclear factor (B (NF-kappaB) in SARS-CoV infected cells. High hydrocortisone concentrations (> or =50 microg/ml) completely prevented increased DNA binding activity of AP-1 and NF-kappaB and inhibited up-regulation of CXCL8 and CXCL10, but did not reduce chemokine expression to basal levels. Ribavirin that does not inhibit SARS-CoV replication in Vero cells inhibited SARS-CoV replication in Caco2 cells at therapeutical concentrations. Hydrocortisone neither influenced SARS-CoV titres alone nor in combination with ribavirin. Our results show that corticosteroids may be of limited benefit in the suppression of chemokine production by SARS-CoV-infected cells.
PubMed: 15647850
Affiliations:
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Le document en format XML
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<term>Chemokine CXCL10</term>
<term>Chemokines (metabolism)</term>
<term>Chemokines, CXC (biosynthesis)</term>
<term>Chlorocebus aethiops</term>
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<term>Up-Regulation</term>
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<term>Antimétabolites (pharmacologie)</term>
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<term>Liaison aux protéines</term>
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<front><div type="abstract" xml:lang="en">Clinical observations and our high-density oligonucleotide microarray results demonstrated increased expression of proinflammatory chemokines after SARS-CoV infection. Here, we investigated the influence of SARS-CoV infection on CXCL8 (interleukin 8) and CXCL10 (interferon-gamma-inducible protein 10) in human intestinal epithelial (Caco2) cells. RT-PCR and ELISA showed time-dependent up-regulation of both chemokines after SARS-CoV infection. Electric mobility shift assay revealed increased DNA binding activity of the cellular transcription factors activator protein 1 (AP-1) and nuclear factor (B (NF-kappaB) in SARS-CoV infected cells. High hydrocortisone concentrations (> or =50 microg/ml) completely prevented increased DNA binding activity of AP-1 and NF-kappaB and inhibited up-regulation of CXCL8 and CXCL10, but did not reduce chemokine expression to basal levels. Ribavirin that does not inhibit SARS-CoV replication in Vero cells inhibited SARS-CoV replication in Caco2 cells at therapeutical concentrations. Hydrocortisone neither influenced SARS-CoV titres alone nor in combination with ribavirin. Our results show that corticosteroids may be of limited benefit in the suppression of chemokine production by SARS-CoV-infected cells.</div>
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<name sortKey="Morgenstern, Birgit" sort="Morgenstern, Birgit" uniqKey="Morgenstern B" first="Birgit" last="Morgenstern">Birgit Morgenstern</name>
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<country name="Allemagne"><region name="Hesse (Land)"><name sortKey="Cinatl, Jindrich" sort="Cinatl, Jindrich" uniqKey="Cinatl J" first="Jindrich" last="Cinatl">Jindrich Cinatl</name>
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