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Interleukin‐11 reduces T‐cell–dependent experimental liver injury in mice
Author(s) -
Bozza Mary,
Bliss Judith L.,
Maylor Richard,
Erickson Jamie,
Donnelly Lori,
Bouchard Page,
Dorner Andrew J.,
Trepicchio William L.
Publication year - 1999
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510300616
Subject(s) - cell injury , liver injury , interleukin , immunology , chemistry , medicine , cytokine , apoptosis , biochemistry
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 γ (IFN‐γ) 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 α (TNF‐α), and IFN‐γ 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.