PMID- 12165091
OWN - NLM
STAT- MEDLINE
DCOM- 20020911
LR  - 20190513
IS  - 0009-9104 (Print)
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Linking)
VI  - 129
IP  - 2
DP  - 2002 Aug
TI  - Interferon-alpha induces interleukin-18 binding protein in chronic hepatitis C 
      patients.
PG  - 332-8
AB  - Interleukin-18 (IL-18), derived from macrophages and Kupffer cells, is the 
      central pro-inflammatory cytokine leading to experimental liver failure. IL-18 
      binding protein (IL-18BP) is a circulating protein that binds IL-18 and 
      neutralizes its activity. Since IL-18 production is increased in chronic HCV 
      infection, we asked whether IFN-alpha might act on the IL-18/IL-18BP system in 
      HCV patients. IL-18BP, total and free IL-18 plasma levels were determined in 13 
      HCV patients receiving 1 x 107 IU IFN-alpha subcutaneously daily for 28 days. The 
      in vitro effects of IFN-alpha on macrophage IL-18BP and IL-18 were studied by 
      enzyme-linked immunosorbent assays and Northern analysis. IFN-alpha 
      administration increased IL-18BP plasma levels 3.24 fold 24 h after institution 
      of therapy, resulting in a 67.4% reduction of free IL-18. Total IL-18 levels 
      decreased from day +24 on. In vitro, IFN-alpha diminished IL-18 release from 
      macrophages of healthy volunteers and chronic HCV patients. On top of its 
      inhibitory effects on IL-1 and TNF-alpha release, IFN-alpha also exerts its 
      anti-inflammatory action in vivo by induction of IL-18BP. These anti-inflammatory 
      properties might account - together with its antiviral action - for its clinical 
      efficacy in chronic hepatitis C.
FAU - Kaser, A
AU  - Kaser A
AD  - Division of Gastroenterology and Hepatology, Department of Medicine, University 
      Hospital Innsbruck, Innsbruck, Austria.
FAU - Novick, D
AU  - Novick D
FAU - Rubinstein, M
AU  - Rubinstein M
FAU - Siegmund, B
AU  - Siegmund B
FAU - Enrich, B
AU  - Enrich B
FAU - Koch, R O
AU  - Koch RO
FAU - Vogel, W
AU  - Vogel W
FAU - Kim, S H
AU  - Kim SH
FAU - Dinarello, C A
AU  - Dinarello CA
FAU - Tilg, H
AU  - Tilg H
LA  - eng
GR  - R01 AI015614/AI/NIAID NIH HHS/United States
GR  - R56 AI015614/AI/NIAID NIH HHS/United States
GR  - AI15614/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (Glycoproteins)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Interferon alpha-2)
RN  - 0 (Interferon-alpha)
RN  - 0 (Interleukin-18)
RN  - 0 (RNA, Messenger)
RN  - 0 (Recombinant Proteins)
RN  - 0 (interleukin-18 binding protein)
SB  - IM
MH  - Down-Regulation/drug effects
MH  - Glycoproteins/*biosynthesis/blood/genetics
MH  - Hepatitis C, Chronic/*drug therapy/genetics/*immunology
MH  - Humans
MH  - In Vitro Techniques
MH  - Intercellular Signaling Peptides and Proteins
MH  - Interferon alpha-2
MH  - Interferon-alpha/*therapeutic use
MH  - Interleukin-18/biosynthesis/blood
MH  - Macrophages/drug effects/immunology
MH  - RNA, Messenger/genetics/metabolism
MH  - Recombinant Proteins
PMC - PMC1906434
EDAT- 2002/08/08 10:00
MHDA- 2002/09/12 10:01
PMCR- 2003/08/01
CRDT- 2002/08/08 10:00
PHST- 2002/08/08 10:00 [pubmed]
PHST- 2002/09/12 10:01 [medline]
PHST- 2002/08/08 10:00 [entrez]
PHST- 2003/08/01 00:00 [pmc-release]
AID - 1911 [pii]
AID - 10.1046/j.1365-2249.2002.01911.x [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2002 Aug;129(2):332-8. doi: 10.1046/j.1365-2249.2002.01911.x.