University of Massachusetts Medical School Faculty Publications


Interleukin-1 inhibition facilitates recovery from liver injury and promotes regeneration of hepatocytes in alcoholic hepatitis in mice

UMMS Affiliation

Department of Medicine, Division of Gastroenterology; Graduate School of Biomedical Sciences, Translational Science Program; UMass Metabolic Network

Publication Date


Document Type



Cell Biology | Cellular and Molecular Physiology | Digestive System Diseases | Gastroenterology | Hepatology


BACKGROUND and AIMS: Inflammation and impaired hepatocyte regeneration contribute to liver failure in alcoholic hepatitis (AH). Interleukin (IL)-1 is a key inflammatory cytokine in the pathobiology of AH. The role of IL-1 in liver regeneration in the recovery phase of alcohol-induced liver injury is unknown.

METHODS: Here we tested IL-1 receptor antagonist to block IL-1 signaling in a mouse model of acute-on-chronic liver injury on liver inflammation and hepatocyte regeneration in AH.

RESULTS: We observed that inhibition of IL-1 signaling decreased liver inflammation, neutrophil infiltration, enhanced regeneration of hepatocytes, and resulted in increased rate of recovery from liver injury in AH.

CONCLUSION: Our novel findings suggest that IL-1 drives sustained liver inflammation and impaired hepatocyte regeneration even after cessation of ethanol exposure.


alcoholic liver disease, interleukin 1, interleukin 1 receptor antagonist, liver regeneration

DOI of Published Version



Liver Int. 2017 Mar 26. doi: 10.1111/liv.13430. Link to article on publisher's site


First author Arvin Iracheta-Vellve is a doctoral student in the Translational Science program in the Graduate School of Biomedical Sciences (GSBS) at UMass Medical School.

Related Resources

Link to Article in PubMed

Journal/Book/Conference Title

Liver international : official journal of the International Association for the Study of the Liver

PubMed ID