IL-33 Induces Nuocytes and Modulates Liver Injury in Viral Hepatitis (original) (raw)
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Department of Microbiology and Immunology, University of Texas Medical Branch
, Galveston, TX 77555
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Department of Microbiology and Immunology, University of Texas Medical Branch
, Galveston, TX 77555
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Department of Microbiology and Immunology, University of Texas Medical Branch
, Galveston, TX 77555
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Department of Microbiology and Immunology, University of Texas Medical Branch
, Galveston, TX 77555
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David Vu ,
Department of Microbiology and Immunology, University of Texas Medical Branch
, Galveston, TX 77555
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Department of Microbiology and Immunology, University of Texas Medical Branch
, Galveston, TX 77555
Department of Pathology, University of Texas Medical Branch
, Galveston, TX 77555
Institute for Human Infections and Immunity, University of Texas Medical Branch
, Galveston, TX 77555
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Department of Microbiology and Immunology, University of Texas Medical Branch
, Galveston, TX 77555
Institute for Human Infections and Immunity, University of Texas Medical Branch
, Galveston, TX 77555
Address correspondence and reprint requests to Dr. Jiaren Sun, Department of Microbiology and Immunology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-1070. E-mail address: [email protected]
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Received:
11 January 2013
Cite
Yuejin Liang, Zuliang Jie, Lifei Hou, Renan Aguilar-Valenzuela, David Vu, Lynn Soong, Jiaren Sun, IL-33 Induces Nuocytes and Modulates Liver Injury in Viral Hepatitis, The Journal of Immunology, Volume 190, Issue 11, June 2013, Pages 5666–5675, https://doi.org/10.4049/jimmunol.1300117
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Abstract
Molecules containing damage-associated molecular patterns play an important role in many pathogenic processes. In this study, our aim was to investigate the role of IL-33, a damage-associated molecular pattern molecule, in adenovirus (Ad)-induced liver inflammation. Ad-infected mice exhibited a steadily increased IL-33 and its receptor IL-1R–like 1 expression in the liver during the first week of infection. Treatment of exogenous IL-33 resulted in a great decrease in the serum alanine aminotransferase levels and the number of Councilman bodies in the liver. Attenuated liver injury by IL-33 correlated with an increase in T regulatory cells but with a decrease in macrophages, dendritic cells, and NK cells in the liver. IL-33 enhanced both type 1 (IL-2 and IFN-γ) and type 2 (IL-5 and IL-13) immune responses in infected mice. However, IL-33 inhibited TNF-α expression in hepatic T cells and macrophages, and significantly reduced TNF-α levels in the liver. We found that in addition to its direct effects, IL-33 strongly induced novel nuocytes in the livers and spleens of infected mice. When cocultured with nuocytes, hepatic T cells and macrophages expressed lower levels of TNF-α. The IL-33–treated mice also demonstrated a slight delay, but no significant impairment, in eliminating an intrahepatic infection with Ad. In conclusion, this study reveals that IL-33 acts as a potent immune stimulator and a hepatoprotective cytokine in acute viral hepatitis. Its direct immunoregulatory functions and ability to induce novel nuocytes further suggest to us that it may be a potentially promising therapeutic candidate for the management of viral hepatitis.
Copyright © 2013 by The American Association of Immunologists, Inc.
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