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* Department of Pathology, Department of Internal Medicine,
§ Division of Pulmonary and Critical Care, and
Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan 48109-0602, USA; and
Department of Medicine, University of Edinburgh, Edinburgh, U.K.
1Correspondence: Department of Pathology, University of Michigan Medical School, 1301 E Catherine, Ann Arbor MI 48109-0602, USA. E-mail: hogaboam{at}path.med.umich.edu
Severe acute liver injury due to accidental or intentional acetaminophen overdose presents a major clinical dilemma often requiring liver transplantation. In the present study, liver regeneration after profound liver injury in mice challenged with acetaminophen was facilitated by the exogenous addition of ELR-containing CXC chemokines such as macrophage inflammatory protein-2 (MIP-2), epithelial neutrophil-activating protein-78 (ENA-78), or interleukin 8. Intravenous administration of ELR-CXC chemokines or N-acetyl-cysteine (NAC) immediately after acetaminophen challenge in mice significantly reduced histological and biochemical markers of hepatic injury. However, when the intervention was delayed until 10 h after acetaminophen challenge, only ELR-CXC chemokines significantly reduced liver injury and mouse mortality. The delayed addition of ELR-CXC chemokines to cultured hepatocytes maintained the proliferation of these cells in a CXCR2-dependent fashion after acetaminophen challenge whereas delayed NAC treatment did not. These observations demonstrate that ELR-CXC chemokines represent novel hepatic regenerative factors that exhibit prolonged therapeutic effects after acetaminophen-induced hepatotoxicity.—Hogaboam, C. M., Bone-Larson, C. L., Steinhauser, M. L., Lukacs, N. W., Colletti, L. M., Simpson, K. J., Strieter, R. M., Kunkel, S. L. Novel CXCR2-dependent liver regenerative qualities of ELR-containing CXC chemokines.
Key Words: acetaminophen • acute liver injury • hepatic regeneration
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