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      Interleukin 18 in the CNS

      review-article
      Author(s): 1 , 2 , 3 , 4 ,
      Publication date (Electronic):
      Journal: Journal of Neuroinflammation
      Publisher: BioMed Central

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          Abstract

          Interleukin (IL)-18 is a cytokine isolated as an important modulator of immune responses and subsequently shown to be pleiotropic. IL-18 and its receptors are expressed in the central nervous system (CNS) where they participate in neuroinflammatory/neurodegenerative processes but also influence homeostasis and behavior. Work on IL-18 null mice, the localization of the IL-18 receptor complex in neurons and the neuronal expression of decoy isoforms of the receptor subunits are beginning to reveal the complexity and the significance of the IL-18 system in the CNS. This review summarizes current knowledge on the central role of IL-18 in health and disease.

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          IL-1, IL-18, and IL-33 families of cytokines.

          William P Arend, Gaby Palmer, Cem Gabay (2008)
          The interleukin-1 (IL-1), IL-18, and IL-33 families of cytokines are related by mechanism of origin, receptor structure, and signal transduction pathways utilized. All three cytokines are synthesized as precursor molecules and cleaved by the enzyme caspase-1 before or during release from the cell. The NALP-3 inflammasome is of crucial importance in generating active caspase-1. The IL-1 family contains two agonists, IL-1alpha and IL-1beta, a specific inhibitor, IL-1 receptor antagonist (IL-1Ra), and two receptors, the biologically active type IL-1R and inactive type II IL-1R. Both IL-1RI and IL-33R utilize the same interacting accessory protein (IL-1RAcP). The balance between IL-1 and IL-1Ra is important in preventing disease in various organs, and excess production of IL-1 has been implicated in many human diseases. The IL-18 family also contains a specific inhibitor, the IL-18-binding protein (IL-18BP), which binds IL-18 in the fluid phase. The IL-18 receptor is similar to the IL-1 receptor complex, including a single ligand-binding chain and a different interacting accessory protein. IL-18 provides an important link between the innate and adaptive immune responses. Newly described IL-33 binds to the orphan IL-1 family receptor T1/ST2 and stimulates T-helper 2 responses as well as mast cells.
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            Activation of interferon-gamma inducing factor mediated by interleukin-1beta converting enzyme.

            Y. Gu, K Kuida, H Tsutsui … (1997)
            The interleukin-1beta (IL-1beta) converting enzyme (ICE) processes the inactive IL-1beta precursor to the proinflammatory cytokine. ICE was also shown to cleave the precursor of interferon-gamma inducing factor (IGIF) at the authentic processing site with high efficiency, thereby activating IGIF and facilitating its export. Lipopolysaccharide-activated ICE-deficient (ICE-/-) Kupffer cells synthesized the IGIF precursor but failed to process it into the active form. Interferon-gamma and IGIF were diminished in the sera of ICE-/- mice exposed to Propionibacterium acnes and lipopolysaccharide. The lack of multiple proinflammatory cytokines in ICE-/- mice may account for their protection from septic shock.
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              Deficiency of interleukin-18 in mice leads to hyperphagia, obesity and insulin resistance.

              Mihai Netea, Ki Kim, M. Baak … (2006)
              Here we report the presence of hyperphagia, obesity and insulin resistance in knockout mice deficient in IL-18 or IL-18 receptor, and in mice transgenic for expression of IL-18 binding protein. Obesity of Il18-/- mice resulted from accumulation of fat tissue based on increased food intake. Il18-/- mice also had hyperinsulinemia, consistent with insulin resistance and hyperglycemia. Insulin resistance was secondary to obesity induced by increased food intake and occurred at the liver level as well as at the muscle and fat-tissue level. The molecular mechanisms responsible for the hepatic insulin resistance in the Il18-/- mice involved an enhanced expression of genes associated with gluconeogenesis in the liver of Il18-/- mice, resulting from defective phosphorylation of STAT3. Recombinant IL-18 (rIL-18) administered intracerebrally inhibited food intake. In addition, rIL-18 reversed hyperglycemia in Il18-/- mice through activation of STAT3 phosphorylation. These findings indicate a new role of IL-18 in the homeostasis of energy intake and insulin sensitivity.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Neuroinflammation
                Title: Journal of Neuroinflammation
                Publisher: BioMed Central
                ISSN (Electronic): 1742-2094
                Publication date Collection: 2010
                Publication date (Electronic): 29 January 2010
                Volume: 7
                Page: 9
                Affiliations
                [1 ]Department of Biomedical Sciences, University of Modena and Reggio Emilia, Italy
                [2 ]Department of Environmental Sciences, University of Tuscia, Viterbo, Italy
                [3 ]Department of Physiology, Nippon Medical School, 1-1-5 Sendagi Bunkyo-ku, Tokyo 113-8602, Japan
                [4 ]Molecular and Integrative Neurosciences Department, The Scripps Research Institute, CA, USA
                Article
                Publisher ID: 1742-2094-7-9
                DOI: 10.1186/1742-2094-7-9
                PMC ID: 2830964
                PubMed ID: 20113500
                SO-VID: c000e752-0c11-4621-a6d9-c27f6c8dcda4
                Copyright © Copyright ©2010 Alboni et al; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 10 December 2009
                Date accepted : 29 January 2010
                Categories
                Subject: Review

                ScienceOpen disciplines: Neurosciences
                Data availability:
                ScienceOpen disciplines: Neurosciences

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