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 language | English (US) |
|---|---|
| Pages (from-to) | 356-361 |
| Number of pages | 6 |
| Journal | Shock |
| Volume | 11 |
| Issue number | 5 |
| DOIs | |
| State | Published - Jan 1 1999 |
| Externally published | Yes |
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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 journal › Article
}
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.
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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 -