Effects of immunomodulation with interferon-γ on hepatic ischemia-reperfusion injury

Lorrie A. Langdale, Lynne Wilson, Gregory Jurkovich, H. Denny Liggitt

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

The development of an inflammatory response after injury depends on the participation of a variety of cell populations and endogenous mediators. Interferon-γ (IFN-γ) is a potent cellular immunomodulating cytokine that contributes to acute and chronic inflammation. In this study, the effects of immunomodulation on ischemia-reperfusion injury were examined using increasing doses of recombinant, rabbit-specific IFN-γ in an in situ model of hepatic ischemia-reperfusion. Pretreatment with low dose IFN-γ augmented injury as measured by histology, aminotransferase concentrations, and myeloperoxidase activity. By contrast, high dose IFN-γ pretreatment, equivalent to IFN-γ supplements used in clinical trials, resulted in a lack of neutrophil infiltration and minimal progression of late phase, neutrophil-mediated reperfusion injury. These results suggest that immunomodulating mediators such as IFN-γ may play a regulating role in the evolution of ischemia-reperfusion, contributing to the development and resolution of acute hepatic injury.

Original languageEnglish (US)
Pages (from-to)356-361
Number of pages6
JournalShock
Volume11
Issue number5
DOIs
StatePublished - Jan 1 1999
Externally publishedYes

Fingerprint

Immunomodulation
Reperfusion Injury
Interferons
Liver
Reperfusion
Wounds and Injuries
Ischemia
Neutrophil Infiltration
Transaminases
Peroxidase
Histology
Neutrophils
Clinical Trials
Cytokines
Rabbits
Inflammation
Population

ASJC Scopus subject areas

  • Emergency Medicine
  • Critical Care and Intensive Care Medicine

Cite this

Effects of immunomodulation with interferon-γ on hepatic ischemia-reperfusion injury. / Langdale, Lorrie A.; Wilson, Lynne; Jurkovich, Gregory; Liggitt, H. Denny.

In: Shock, Vol. 11, No. 5, 01.01.1999, p. 356-361.

Research output: Contribution to journalArticle

Langdale, Lorrie A. ; Wilson, Lynne ; Jurkovich, Gregory ; Liggitt, H. Denny. / Effects of immunomodulation with interferon-γ on hepatic ischemia-reperfusion injury. In: Shock. 1999 ; Vol. 11, No. 5. pp. 356-361.
@article{6ed6e787609c4185a24b13aa70d14ffc,
title = "Effects of immunomodulation with interferon-γ on hepatic ischemia-reperfusion injury",
abstract = "The development of an inflammatory response after injury depends on the participation of a variety of cell populations and endogenous mediators. Interferon-γ (IFN-γ) is a potent cellular immunomodulating cytokine that contributes to acute and chronic inflammation. In this study, the effects of immunomodulation on ischemia-reperfusion injury were examined using increasing doses of recombinant, rabbit-specific IFN-γ in an in situ model of hepatic ischemia-reperfusion. Pretreatment with low dose IFN-γ augmented injury as measured by histology, aminotransferase concentrations, and myeloperoxidase activity. By contrast, high dose IFN-γ pretreatment, equivalent to IFN-γ supplements used in clinical trials, resulted in a lack of neutrophil infiltration and minimal progression of late phase, neutrophil-mediated reperfusion injury. These results suggest that immunomodulating mediators such as IFN-γ may play a regulating role in the evolution of ischemia-reperfusion, contributing to the development and resolution of acute hepatic injury.",
author = "Langdale, {Lorrie A.} and Lynne Wilson and Gregory Jurkovich and Liggitt, {H. Denny}",
year = "1999",
month = "1",
day = "1",
doi = "10.1097/00024382-199905000-00009",
language = "English (US)",
volume = "11",
pages = "356--361",
journal = "Shock",
issn = "1073-2322",
publisher = "Lippincott Williams and Wilkins",
number = "5",

}

TY - JOUR

T1 - Effects of immunomodulation with interferon-γ on hepatic ischemia-reperfusion injury

AU - Langdale, Lorrie A.

AU - Wilson, Lynne

AU - Jurkovich, Gregory

AU - Liggitt, H. Denny

PY - 1999/1/1

Y1 - 1999/1/1

N2 - The development of an inflammatory response after injury depends on the participation of a variety of cell populations and endogenous mediators. Interferon-γ (IFN-γ) is a potent cellular immunomodulating cytokine that contributes to acute and chronic inflammation. In this study, the effects of immunomodulation on ischemia-reperfusion injury were examined using increasing doses of recombinant, rabbit-specific IFN-γ in an in situ model of hepatic ischemia-reperfusion. Pretreatment with low dose IFN-γ augmented injury as measured by histology, aminotransferase concentrations, and myeloperoxidase activity. By contrast, high dose IFN-γ pretreatment, equivalent to IFN-γ supplements used in clinical trials, resulted in a lack of neutrophil infiltration and minimal progression of late phase, neutrophil-mediated reperfusion injury. These results suggest that immunomodulating mediators such as IFN-γ may play a regulating role in the evolution of ischemia-reperfusion, contributing to the development and resolution of acute hepatic injury.

AB - The development of an inflammatory response after injury depends on the participation of a variety of cell populations and endogenous mediators. Interferon-γ (IFN-γ) is a potent cellular immunomodulating cytokine that contributes to acute and chronic inflammation. In this study, the effects of immunomodulation on ischemia-reperfusion injury were examined using increasing doses of recombinant, rabbit-specific IFN-γ in an in situ model of hepatic ischemia-reperfusion. Pretreatment with low dose IFN-γ augmented injury as measured by histology, aminotransferase concentrations, and myeloperoxidase activity. By contrast, high dose IFN-γ pretreatment, equivalent to IFN-γ supplements used in clinical trials, resulted in a lack of neutrophil infiltration and minimal progression of late phase, neutrophil-mediated reperfusion injury. These results suggest that immunomodulating mediators such as IFN-γ may play a regulating role in the evolution of ischemia-reperfusion, contributing to the development and resolution of acute hepatic injury.

UR - http://www.scopus.com/inward/record.url?scp=0033128517&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033128517&partnerID=8YFLogxK

U2 - 10.1097/00024382-199905000-00009

DO - 10.1097/00024382-199905000-00009

M3 - Article

C2 - 10353542

AN - SCOPUS:0033128517

VL - 11

SP - 356

EP - 361

JO - Shock

JF - Shock

SN - 1073-2322

IS - 5

ER -