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      • Record: found
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      Downregulation of the NLRP3 inflammasome by adiponectin rescues Duchenne muscular dystrophy.

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          Abstract

          The hormone adiponectin (ApN) exerts powerful anti-inflammatory effects on skeletal muscle and can reverse devastating myopathies, like Duchenne muscular dystrophy (DMD), where inflammation exacerbates disease progression. The NLRP3 inflammasome plays a key role in the inflammation process, and its aberrant activation leads to several inflammatory or immune diseases. Here we investigated the expression of the NLRP inflammasome in skeletal muscle and its contribution to DMD.

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          NLRP3 inflammasome and its inhibitors: a review

          Bo-zong Shao, Zhe-Qi Xu, Bin-ze Han … (2015)
          Inflammasomes are newly recognized, vital players in innate immunity. The best characterized is the NLRP3 inflammasome, so-called because the NLRP3 protein in the complex belongs to the family of nucleotide-binding and oligomerization domain-like receptors (NLRs) and is also known as “pyrin domain-containing protein 3”. The NLRP3 inflammasome is associated with onset and progression of various diseases, including metabolic disorders, multiple sclerosis, inflammatory bowel disease, cryopyrin-associated periodic fever syndrome, as well as other auto-immune and auto-inflammatory diseases. Several NLRP3 inflammasome inhibitors have been described, some of which show promise in the clinic. The present review will describe the structure and mechanisms of activation of the NLRP3 inflammasome, its association with various auto-immune and auto-inflammatory diseases, and the state of research into NLRP3 inflammasome inhibitors.
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            Adiponectin as an anti-inflammatory factor.

            Noriyuki Ouchi, Kenneth Walsh (2007)
            Obesity is characterized by low-grade systemic inflammation. Adiponectin is an adipose tissue-derived hormone, which is downregulated in obesity. Adiponectin displays protective actions on the development of various obesity-linked diseases. Several clinical studies demonstrate the inverse relationship between plasma adiponectin levels and several inflammatory markers including C-reactive protein. Adiponectin attenuates inflammatory responses to multiple stimuli by modulating signaling pathways in a variety of cell types. The anti-inflammatory properties of adiponectin may be a major component of its beneficial effects on cardiovascular and metabolic disorders including atherosclerosis and insulin resistance. In this review, we focus on the role of adiponectin in regulation of inflammatory response and discuss its potential as an anti-inflammatory marker.
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              FADD and caspase-8 mediate priming and activation of the canonical and noncanonical Nlrp3 inflammasomes.

              Prajwal Gurung, Paras K. Anand, R. K. Subbarao Malireddi … (2014)
              The Nlrp3 inflammasome is critical for host immunity, but the mechanisms controlling its activation are enigmatic. In this study, we show that loss of FADD or caspase-8 in a RIP3-deficient background, but not RIP3 deficiency alone, hampered transcriptional priming and posttranslational activation of the canonical and noncanonical Nlrp3 inflammasome. Deletion of caspase-8 in the presence or absence of RIP3 inhibited caspase-1 and caspase-11 activation by Nlrp3 stimuli but not the Nlrc4 inflammasome. In addition, FADD deletion prevented caspase-8 maturation, positioning FADD upstream of caspase-8. Consequently, FADD- and caspase-8-deficient mice had impaired IL-1β production when challenged with LPS or infected with the enteropathogen Citrobacter rodentium. Thus, our results reveal FADD and caspase-8 as apical mediators of canonical and noncanonical Nlrp3 inflammasome priming and activation.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): BMC Biol
                Title: BMC biology
                Publisher: Springer Science and Business Media LLC
                ISSN (Electronic): 1741-7007
                ISSN (Print): 1741-7007
                Publication date (Electronic): March 20 2018
                Volume: 16
                Issue: 1
                Affiliations
                [1 ] Endocrinology, Diabetes and Nutrition Unit, Institute of Experimental and Clinical Research, Medical Sector, Catholic University of Louvain, 1200, Brussels, Belgium.
                [2 ] Endocrinology, Diabetes and Nutrition Unit, Institute of Experimental and Clinical Research, Medical Sector, Catholic University of Louvain, 1200, Brussels, Belgium. sonia.brichard@uclouvain.be.
                [3 ] IREC - Endocrinology, Diabetes and Nutrition Unit, UCL/EDIN B1.55.06 - Av. Hippocrate 55, Harvey 55, B-1200, Brussels, Belgium. sonia.brichard@uclouvain.be.
                Article
                Publisher Item ID: 10.1186/s12915-018-0501-z
                DOI: 10.1186/s12915-018-0501-z
                PMC ID: 5861675
                PubMed ID: 29558930
                SO-VID: df8a0be4-6484-4ffa-a4f7-204475b157b8
                History

                Keywords: Duchenne muscular dystrophy,Adiponectin,Inflammation,NLRP3 inflammasome,Skeletal muscle,miR-711
                Data availability:
                Keywords: Duchenne muscular dystrophy, Adiponectin, Inflammation, NLRP3 inflammasome, Skeletal muscle, miR-711

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