PMID- 13680216
OWN - NLM
STAT- MEDLINE
DCOM- 20040727
LR  - 20181130
IS  - 0300-8584 (Print)
IS  - 0300-8584 (Linking)
VI  - 193
IP  - 2-3
DP  - 2004 May
TI  - Interferons in enteroviral heart disease: modulation of cytokine expression and 
      antiviral activity.
PG  - 149-54
AB  - Interferon (IFN)-beta has a more than 120-fold higher antiviral activity than the 
      closely related IFN-alpha in human myocardial fibroblasts infected with the 
      cardiotropic enterovirus coxsackievirus B3 (CVB3). CVB3 replication induces 
      interleukin (IL)-6 and IL-8 expression in myocardial fibroblasts, and suppresses 
      the expression of monocyte chemoattractant protein-1 (MCP-1). We investigated 
      whether the higher antiviral activity of IFN-beta compared to IFN-alpha was a 
      result of a suppression of IL-8 expression by IFN-beta since previous studies had 
      indicated that IL-8 stimulates enterovirus replication. Human myocardial 
      fibroblasts were treated with either IFN-alpha, IFN-beta or IFN-gamma (0, 10, 
      100, or 1,000 IU/ml) and the concentrations of IL-6, IL-8 and MCP-1 were measured 
      in culture supernatants by immunoassays. Both IFN-beta and IFN-gamma reduced IL-6 
      and IL-8 expression significantly. In addition, neutralization of IL-8 in culture 
      supernatants of myocardial fibroblasts using a monoclonal antibody demonstrated a 
      significant reduction of CVB3 titers. Antiproliferative effects of all three IFNs 
      were very low (<30% with 1,000 IU/ml), indicating that the suppression IL-6 and 
      IL-8 was not related to cytotoxicity. MCP-1 expression was increased only by high 
      concentrations of IFN-gamma (1,000 IU/ml). By contrast, IFN-alpha had no 
      significant effect on IL-6, IL-8 and MCP-1 expression. In conclusion, suppression 
      of IL-8 expression is an "immuno-modulating" feature of IFN-beta in human 
      myocardial fibroblasts, which is similar to the activity of IFN-gamma. This 
      feature of IFN-beta contributes to its high antiviral activity against CVB3 and 
      may be useful in the treatment of enteroviral heart disease.
FAU - Heim, Albert
AU  - Heim A
AD  - Institut fur Virologie, Medizinische Hochschule Hannover, Carl-Neuberg-Str. 1, 
      30625 Hannover, Germany. ahei@virologie.mh-hannover.de
FAU - Weiss, Sabine
AU  - Weiss S
LA  - eng
PT  - Journal Article
DEP - 20030912
PL  - Germany
TA  - Med Microbiol Immunol
JT  - Medical microbiology and immunology
JID - 0314524
RN  - 0 (Antiviral Agents)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Interferon Type I)
RN  - 0 (Interferon alpha-2)
RN  - 0 (Interferon-alpha)
RN  - 0 (Interleukin-6)
RN  - 0 (Interleukin-8)
RN  - 0 (Recombinant Proteins)
RN  - 82115-62-6 (Interferon-gamma)
RN  - 9008-11-1 (Interferons)
SB  - IM
MH  - Antiviral Agents/*pharmacology
MH  - Cells, Cultured
MH  - Chemokine CCL2/metabolism
MH  - Cytokines/drug effects/*metabolism
MH  - Enterovirus B, Human/drug effects/*pathogenicity
MH  - Fibroblasts/*virology
MH  - Humans
MH  - Interferon Type I/pharmacology
MH  - Interferon alpha-2
MH  - Interferon-alpha/pharmacology
MH  - Interferon-gamma/pharmacology
MH  - Interferons/genetics/*pharmacology
MH  - Interleukin-6/metabolism
MH  - Interleukin-8/metabolism
MH  - Myocardium/*cytology
MH  - Recombinant Proteins
EDAT- 2003/09/19 05:00
MHDA- 2004/07/28 05:00
CRDT- 2003/09/19 05:00
PHST- 2003/03/27 00:00 [received]
PHST- 2003/09/19 05:00 [pubmed]
PHST- 2004/07/28 05:00 [medline]
PHST- 2003/09/19 05:00 [entrez]
AID - 10.1007/s00430-003-0200-3 [doi]
PST - ppublish
SO  - Med Microbiol Immunol. 2004 May;193(2-3):149-54. doi: 10.1007/s00430-003-0200-3. 
      Epub 2003 Sep 12.