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      Update of inflammasome activation in microglia/macrophage in aging and aging‐related disease

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          Abstract

          Aging and aging‐related CNS diseases are associated with inflammatory status. As an efficient amplifier of immune responses, inflammasome is activated and played detrimental role in aging and aging‐related CNS diseases. Macrophage and microglia display robust inflammasome activation in infectious and sterile inflammation. This review discussed the impact of inflammasome activation in microglia/macrophage on senescence “inflammaging” and aging‐related CNS diseases. The preventive or therapeutic effects of targeting inflammasome on retarding aging process or tackling aging‐related diseases are also discussed.

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          Recent advances in the mechanisms of NLRP3 inflammasome activation and its inhibitors

          Yang Yang, Huanan Wang, Mohammed Kouadir … (2019)
          The NLRP3 inflammasome is a multimeric protein complex that initiates an inflammatory form of cell death and triggers the release of proinflammatory cytokines IL-1β and IL-18. The NLRP3 inflammasome has been implicated in a wide range of diseases, including Alzheimer’s disease, Prion diseases, type 2 diabetes, and some infectious diseases. It has been found that a variety of stimuli including danger-associated molecular patterns (DAMPs, such as silica and uric acid crystals) and pathogen-associated molecular patterns (PAMPs) can activate NLRP3 inflammasome, but the specific regulatory mechanisms of NLRP3 inflammasome activation remain unclear. Understanding the mechanisms of NLRP3 activation will enable the development of its specific inhibitors to treat NLRP3-related diseases. In this review, we summarize current understanding of the regulatory mechanisms of NLRP3 inflammasome activation as well as inhibitors that specifically and directly target NLRP3.
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            Dopamine controls systemic inflammation through inhibition of NLRP3 inflammasome.

            Yiqing Yan, Wei Jiang, Lei Liu … (2015)
            Inflammasomes are involved in diverse inflammatory diseases, so the activation of inflammasomes needs to be tightly controlled to prevent excessive inflammation. However, the endogenous regulatory mechanisms of inflammasome activation are still unclear. Here, we report that the neurotransmitter dopamine (DA) inhibits NLRP3 inflammasome activation via dopamine D1 receptor (DRD1). DRD1 signaling negatively regulates NLRP3 inflammasome via a second messenger cyclic adenosine monophosphate (cAMP), which binds to NLRP3 and promotes its ubiquitination and degradation via the E3 ubiquitin ligase MARCH7. Importantly, in vivo data show that DA and DRD1 signaling prevent NLRP3 inflammasome-dependent inflammation, including neurotoxin-induced neuroinflammation, LPS-induced systemic inflammation, and monosodium urate crystal (MSU)-induced peritoneal inflammation. Taken together, our results reveal an endogenous mechanism of inflammasome regulation and suggest DRD1 as a potential target for the treatment of NLRP3 inflammasome-driven diseases.
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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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                Author and article information

                Contributors
                Zheng‐qi Lu: lzq1828@outlook.com
                Wei Cai:
                ORCID: https://orcid.org/0000-0003-4059-4627
                jchoigz@outlook.com
                Journal
                Journal ID (nlm-ta): CNS Neurosci Ther
                Journal ID (iso-abbrev): CNS Neurosci Ther
                Journal ID (doi): 10.1111/(ISSN)1755-5949
                Journal ID (publisher-id): CNS
                Title: CNS Neuroscience & Therapeutics
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 1755-5930
                ISSN (Electronic): 1755-5949
                Publication date (Electronic): 14 November 2019
                Publication date Collection: December 2019
                Volume: 25
                Issue: 12 , Special Issue on Microglia/macrophage diversities in CNS injuries and diseases ( doiID: 10.1111/cns.v25.12 )
                Pages: 1299-1307
                Affiliations
                [ 1 ] Department of Neurology Center for Mental and Neurological Disorders and Diseases The Third Affiliated Hospital of Sun Yat‐sen University Guangzhou China
                [ 2 ] Center of Clinical Immunology Center for Mental and Neurological Disorders and Diseases The Third Affiliated Hospital of Sun Yat‐sen University Guangzhou China
                Author notes
                [*] [* ] Correspondence

                Wei Cai and Zheng‐qi Lu, Department of Neurology, Center for Mental and Neurological Disorders and Diseases, The Third Affiliated Hospital of Sun Yat‐sen University, 600 Tianhe Road, Guangzhou, Guangdong 510630, China.

                Email: jchoigz@ 123456outlook.com (W. C.); lzq1828@ 123456outlook.com (Z. L.)

                Author information
                https://orcid.org/0000-0003-4059-4627
                Article
                Publisher ID: CNS13262
                DOI: 10.1111/cns.13262
                PMC ID: 6887669
                PubMed ID: 31729181
                SO-VID: 667838e0-94d8-49c9-8f3f-c808c200e89e
                Copyright © © 2019 The Authors. CNS Neuroscience & Therapeutics Published by John Wiley & Sons Ltd.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 27 September 2019
                Date revision received : 21 October 2019
                Date accepted : 24 October 2019
                Page count
                Figures: 4, Tables: 0, Pages: 18, Words: 6169
                Funding
                Funded by: China Postdoctoral Science Foundation , open-funder-registry 10.13039/501100002858;
                Award ID: 2018M643332
                Funded by: Chinese Natural Science Foundation (NCSF)
                Award ID: 81671178
                Categories
                Subject: Review Article
                Subject: Review Articles
                Custom metadata
                source-schema-version-number 2.0
                cover-date December 2019
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:5.7.2 mode:remove_FC converted:03.12.2019

                ScienceOpen disciplines: Neurosciences
                Keywords: aging,inflammasome,inflammation,macrophage,microglia
                Data availability:
                ScienceOpen disciplines: Neurosciences
                Keywords: aging, inflammasome, inflammation, macrophage, microglia

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