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Interleukin-11 reduces T-cell–dependent experimental liver injury in mice

✍ Scribed by Mary Bozza; Judith L. Bliss; Richard Maylor; Jamie Erickson; Lori Donnelly; Page Bouchard; Andrew J. Dorner; William L. Trepicchio

Publisher
John Wiley and Sons
Year
1999
Tongue
English
Weight
544 KB
Volume
30
Category
Article
ISSN
0270-9139

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✦ Synopsis

Recombinant human interleukin-11 (rhIL-11) is a multifunctional cytokine that can reduce inflammation through the downregulation of multiple pro-inflammatory mediators from activated macrophages. rhIL-11 also inhibits production of several immunostimulatory cytokines such as IL-12 and interferon ␥ (IFN-␥) and has shown biological activity in multiple animal models of inflammatory disease consistent with immunomodulatory effects on macrophages and T cells. To further elucidate the anti-inflammatory activity of rhIL-11 in vivo, the effect of rhIL-11 in a model of Concanavalin A (Con-A)-induced T-cell-mediated hepatotoxicity was examined. Administration of a single dose of rhIL-11 before Con-A administration reduced centrilobular liver necrosis and enhanced survival. A dose-dependent reduction in serum levels of liver enzymes, tumor necrosis factor ␣ (TNF-␣), and IFN-␥ corresponded with this amelioration of liver damage. No significant change in infiltrating lymphocyte populations in the liver was observed following rhIL-11 treatment. Taken together, these results indicate that rhIL-11 ameliorates T-cell-mediated hepatic injury and suggests its therapeutic potential to treat inflammatory liver disease. (HEPATOLOGY 1999;30:1441-1447.)

Methods

Con-A-Induced Hepatitis. All experiments were performed using protocols approved by the Genetics Institute Animal Care Use

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