High-dose hydrocortisone reduces expression of the pro-inflammatory chemokines CXCL8 and CXCL10 in SARS coronavirus-infected intestinal cells

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.

Medienart:

Artikel

Erscheinungsjahr:

2005

Erschienen:

2005

Enthalten in:

Zur Gesamtaufnahme - volume:15

Enthalten in:

International journal of molecular medicine - 15(2005), 2 vom: 27. Feb., Seite 323-7

Sprache:

Englisch

Beteiligte Personen:

Cinatl, Jindrich [VerfasserIn]
Michaelis, Martin [VerfasserIn]
Morgenstern, Birgit [VerfasserIn]
Doerr, Hans Wilhelm [VerfasserIn]

Themen:

49717AWG6K
9007-49-2
Anti-Inflammatory Agents
Antimetabolites
CXCL10 protein, human
Chemokine CXCL10
Chemokines
Chemokines, CXC
DNA
Hydrocortisone
Interleukin-8
Journal Article
Ribavirin
WI4X0X7BPJ

Anmerkungen:

Date Completed 08.08.2005

Date Revised 07.12.2022

published: Print

Citation Status MEDLINE

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM153084642