Type I, but not type II, interferon is critical in liver injury induced after ischemia and reperfusion.

Type I, but not type II, interferon is critical in liver injury induced after ischemia and reperfusion. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Type I, but not type II, interferon is critical in liver injury induced after ischemia and reperfusion. Abstract Text:

Yuan Zhai,Bo Qiao,Feng Gao,Xiuda Shen,Andrew Vardanian,Ronald W Busuttil,Jerzy W Kupiec-Weglinski,Yuan Zhai,Bo Qiao,Feng Gao,Xiuda Shen,Andrew Vardanian,Ronald W Busuttil,Jerzy W Kupiec-Weglinski,

We have documented the key role of toll-like receptor 4 (TLR4) activation and its signaling pathway mediated by interferon (IFN) regulatory factor 3, in the induction of inflammation leading to the hepatocellular damage during liver ischemia/reperfusion injury (IRI). Because type I IFN is the major downstream activation product of that pathway, we studied its role in comparison with IFN-gamma. Groups of type I (IFNAR), type II (IFNGR) IFN receptor-deficient mice, along with wild-type (WT) controls were subjected to partial liver warm ischemia (90 minutes) followed by reperfusion (1-6 hours). Interestingly, IFNAR knockout (KO) but not IFNGR KO mice were protected from IR-induced liver damage, as evidenced by decreased serum alanine aminotransferase and preservation of tissue architecture. IR-triggered intrahepatic pro-inflammatory response, assessed by tumor necrosis factor (TNF-alpha), interleukin 6 (IL-6), and chemokine (C-X-C motif) ligand 10 (CXCL-10) expression, was diminished selectively in IFNAR KO mice. Consistent with these findings, our in vitro cell culture studies have shown that: (1) although hepatocytes alone failed to respond to lipopolysaccharide (LPS), when co-cultured with macrophages they did respond to LPS via macrophage-derived IFN-beta; (2) macrophages required type I IFN to sustain CXCL10 production in response to LPS. This study documents that type I, but not type II, IFN pathway is required for IR-triggered liver inflammation/damage. Type I IFN mediates potential synergy between nonparenchyma and parenchyma cells in response to TLR4 activation. (HEPATOLOGY 2007.).

Type I, but not type II, interferon is critical in liver injury induced after ischemia and reperfusion. Publishing Authors By Initials

Y Zhai,B Qiao,F Gao,X Shen,A Vardanian,RW Busuttil,JW Kupiec-Weglinski,Y Zhai,B Qiao,F Gao,X Shen,A Vardanian,RW Busuttil,JW Kupiec-Weglinski,

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

Type I, but not type II, interferon is critical in liver injury induced after ischemia and reperfusion. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Hepatology (Baltimore, Md.)

VOLUME: 47

Page Numbers: 199-206

Journal Abbreviation: Hepatology

ISSN: 1527-3350

DAY: 2

MONTH: Jan

YEAR: 2008

Type I, but not type II, interferon is critical in liver injury induced after ischemia and reperfusion. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8302946

Type I, but not type II, interferon is critical in liver injury induced after ischemia and reperfusion. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: Type I, but not type II, interferon is critical in liver injury induced after ischemia and reperfusion. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Type I, but not type II, interferon is critical in liver injury induced after ischemia and reperfusion.

AFFILIATION: Dumont-UCLA Transplant Center, Department of Surgery, Division of Liver and Pancreas Transplantation, David Geffen School of Medicine at UCLA, Los Angeles, CA.

Country: United States

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: Hepatology

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Type I, but not type II, interferon is critical in liver injury induced after ischemia and reperfusion Related Publications

• Absence of toll-like receptor 4 (TLR4) signaling in the donor organ reduces ischemia and reperfusion injury in a murine liver transplantation model.
• CXCL10 regulates liver innate immune response against ischemia and reperfusion injury.
• Critical role of CD4 help in CD154 blockade-resistant memory CD8 T cell activation and allograft rejection in sensitized recipients.
• Defective alloreactive CD8 T cell function and memory response in allograft recipients in the absence of CD4 help.
• Diannexin, a novel annexin V homodimer, protects rat liver transplants against cold ischemia-reperfusion injury.
• Differential impact of CD154 costimulation blockade on alloreactive effector and regulatory T cells in murine renal transplant recipients.
• Molecular mediators of liver ischemia and reperfusion injury: a brief review.
• Tolerance induction.
• Type I, but not type II, interferon is critical in liver injury induced after ischemia and reperfusion.
• Viral interleukin-10 gene transfer prevents liver ischemia-reperfusion injury: Toll-like receptor-4 and heme oxygenase-1 signaling in innate and adaptive immunity.