NLRP3 inflammasome in sepsis (Review)
Sepsis is an imbalanced response to infection that leads to life-threatening organ dysfunction. Although an increasing number of anti-inflammatory drugs are available, the options for treating sepsis remain limited. Therefore, it is imperative to understand the pathogenesis and pathophysiology of se...
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| Veröffentlicht in: | Molecular medicine reports 2021-07, Vol.24 (1), Article 514 |
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| creator | Shi, Xueyan Tan, Sichuang Tan, Sipin |
| description | Sepsis is an imbalanced response to infection that leads to life-threatening organ dysfunction. Although an increasing number of anti-inflammatory drugs are available, the options for treating sepsis remain limited. Therefore, it is imperative to understand the pathogenesis and pathophysiology of sepsis and develop novel therapeutic targets to treat this state. The Nod-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is a cytoplasmic high-molecular weight protein complex composed of the sensor NLRP3, adapter protein apoptosis-related speck-like protein and pro-caspase-1. It functions by cleaving pro-caspase-1 to become active caspase-1, resulting in the maturation and release of IL-1β and IL-18. Activation of the NLRP3 inflammasome is necessary for innate immune defense and also serves an important role in adaptive immune responses. Studies have shown that the NLRP3 inflammasome is involved in the occurrence and evolution of sepsis and other immune inflammatory diseases. The present paper reviews the activation pathways and biological function of the NLRP3 inflammasome in sepsis, with the aim to provide a basis for further research. |
| doi_str_mv | 10.3892/mmr.2021.12153 |
| format | Article |
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Although an increasing number of anti-inflammatory drugs are available, the options for treating sepsis remain limited. Therefore, it is imperative to understand the pathogenesis and pathophysiology of sepsis and develop novel therapeutic targets to treat this state. The Nod-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is a cytoplasmic high-molecular weight protein complex composed of the sensor NLRP3, adapter protein apoptosis-related speck-like protein and pro-caspase-1. It functions by cleaving pro-caspase-1 to become active caspase-1, resulting in the maturation and release of IL-1β and IL-18. Activation of the NLRP3 inflammasome is necessary for innate immune defense and also serves an important role in adaptive immune responses. Studies have shown that the NLRP3 inflammasome is involved in the occurrence and evolution of sepsis and other immune inflammatory diseases. The present paper reviews the activation pathways and biological function of the NLRP3 inflammasome in sepsis, with the aim to provide a basis for further research.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2021.12153</identifier><identifier>PMID: 33982766</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Adaptive immunity ; Anti-inflammatory agents ; Apoptosis ; Atherosclerosis ; Care and treatment ; Caspase-1 ; Cellular signal transduction ; Cytokines ; Cytoplasm ; Development and progression ; Drug development ; Health aspects ; IL-1β ; Immune response ; Immune system ; Immunosuppressive agents ; Infections ; Inflammasomes ; Inflammatory diseases ; Interleukin 18 ; Microorganisms ; Mitochondrial DNA ; Molecular weight ; Mortality ; Pathogenesis ; Pathogens ; Pathophysiology ; Pattern recognition ; Proteins ; Pyrin protein ; Sepsis ; Therapeutic targets</subject><ispartof>Molecular medicine reports, 2021-07, Vol.24 (1), Article 514</ispartof><rights>COPYRIGHT 2021 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2021</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c430t-f291a5dae550a5494b713528716596968867061876c0c1b0c26c05034b38c1443</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33982766$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shi, Xueyan</creatorcontrib><creatorcontrib>Tan, Sichuang</creatorcontrib><creatorcontrib>Tan, Sipin</creatorcontrib><title>NLRP3 inflammasome in sepsis (Review)</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Sepsis is an imbalanced response to infection that leads to life-threatening organ dysfunction. Although an increasing number of anti-inflammatory drugs are available, the options for treating sepsis remain limited. Therefore, it is imperative to understand the pathogenesis and pathophysiology of sepsis and develop novel therapeutic targets to treat this state. The Nod-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is a cytoplasmic high-molecular weight protein complex composed of the sensor NLRP3, adapter protein apoptosis-related speck-like protein and pro-caspase-1. It functions by cleaving pro-caspase-1 to become active caspase-1, resulting in the maturation and release of IL-1β and IL-18. Activation of the NLRP3 inflammasome is necessary for innate immune defense and also serves an important role in adaptive immune responses. Studies have shown that the NLRP3 inflammasome is involved in the occurrence and evolution of sepsis and other immune inflammatory diseases. The present paper reviews the activation pathways and biological function of the NLRP3 inflammasome in sepsis, with the aim to provide a basis for further research.</description><subject>Adaptive immunity</subject><subject>Anti-inflammatory agents</subject><subject>Apoptosis</subject><subject>Atherosclerosis</subject><subject>Care and treatment</subject><subject>Caspase-1</subject><subject>Cellular signal transduction</subject><subject>Cytokines</subject><subject>Cytoplasm</subject><subject>Development and progression</subject><subject>Drug development</subject><subject>Health aspects</subject><subject>IL-1β</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunosuppressive agents</subject><subject>Infections</subject><subject>Inflammasomes</subject><subject>Inflammatory diseases</subject><subject>Interleukin 18</subject><subject>Microorganisms</subject><subject>Mitochondrial DNA</subject><subject>Molecular weight</subject><subject>Mortality</subject><subject>Pathogenesis</subject><subject>Pathogens</subject><subject>Pathophysiology</subject><subject>Pattern recognition</subject><subject>Proteins</subject><subject>Pyrin protein</subject><subject>Sepsis</subject><subject>Therapeutic targets</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkc9LwzAUx4Mobk6vHmUgwjy0JnlN0hzH8BcMlaHnkGapdDTtTFbF_95UpwdZ3iHvhc_78g1fhE4JTiGX9Mo5n1JMSUooYbCHhkRIkgDG2f62p1KKAToKYYUxZ5TJQzQAkDkVnA_RxcN88QTjqilr7ZwOrbNxGAe7DlUYTxb2vbIfl8fooNR1sCfbe4Rebq6fZ3fJ_PH2fjadJyYDvElKKolmS20Zw5plMisEAUZzQTiTXPI85wJzkgtusCEFNjQ2DENWQG5IlsEITX50175962zYKFcFY-taN7btgqKMcsCMSxHR83_oqu18E91FCriIalH5j3rVtVXxl-3Ga9OLqimPJzqDnkp3ULGW1lWmbWxZxfddC8a3IXhbqrWvnPafimDV56JiLqrPRX3nEhfOtm67wtnlH_4bBHwBrgOB2w</recordid><startdate>20210701</startdate><enddate>20210701</enddate><creator>Shi, Xueyan</creator><creator>Tan, Sichuang</creator><creator>Tan, Sipin</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20210701</creationdate><title>NLRP3 inflammasome in sepsis (Review)</title><author>Shi, Xueyan ; Tan, Sichuang ; Tan, Sipin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c430t-f291a5dae550a5494b713528716596968867061876c0c1b0c26c05034b38c1443</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adaptive immunity</topic><topic>Anti-inflammatory agents</topic><topic>Apoptosis</topic><topic>Atherosclerosis</topic><topic>Care and treatment</topic><topic>Caspase-1</topic><topic>Cellular signal transduction</topic><topic>Cytokines</topic><topic>Cytoplasm</topic><topic>Development and progression</topic><topic>Drug development</topic><topic>Health aspects</topic><topic>IL-1β</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Immunosuppressive agents</topic><topic>Infections</topic><topic>Inflammasomes</topic><topic>Inflammatory diseases</topic><topic>Interleukin 18</topic><topic>Microorganisms</topic><topic>Mitochondrial DNA</topic><topic>Molecular weight</topic><topic>Mortality</topic><topic>Pathogenesis</topic><topic>Pathogens</topic><topic>Pathophysiology</topic><topic>Pattern recognition</topic><topic>Proteins</topic><topic>Pyrin protein</topic><topic>Sepsis</topic><topic>Therapeutic targets</topic><toplevel>online_resources</toplevel><creatorcontrib>Shi, Xueyan</creatorcontrib><creatorcontrib>Tan, Sichuang</creatorcontrib><creatorcontrib>Tan, Sipin</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shi, Xueyan</au><au>Tan, Sichuang</au><au>Tan, Sipin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>NLRP3 inflammasome in sepsis (Review)</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2021-07-01</date><risdate>2021</risdate><volume>24</volume><issue>1</issue><artnum>514</artnum><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Sepsis is an imbalanced response to infection that leads to life-threatening organ dysfunction. Although an increasing number of anti-inflammatory drugs are available, the options for treating sepsis remain limited. Therefore, it is imperative to understand the pathogenesis and pathophysiology of sepsis and develop novel therapeutic targets to treat this state. The Nod-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is a cytoplasmic high-molecular weight protein complex composed of the sensor NLRP3, adapter protein apoptosis-related speck-like protein and pro-caspase-1. It functions by cleaving pro-caspase-1 to become active caspase-1, resulting in the maturation and release of IL-1β and IL-18. Activation of the NLRP3 inflammasome is necessary for innate immune defense and also serves an important role in adaptive immune responses. Studies have shown that the NLRP3 inflammasome is involved in the occurrence and evolution of sepsis and other immune inflammatory diseases. 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| subjects | Adaptive immunity Anti-inflammatory agents Apoptosis Atherosclerosis Care and treatment Caspase-1 Cellular signal transduction Cytokines Cytoplasm Development and progression Drug development Health aspects IL-1β Immune response Immune system Immunosuppressive agents Infections Inflammasomes Inflammatory diseases Interleukin 18 Microorganisms Mitochondrial DNA Molecular weight Mortality Pathogenesis Pathogens Pathophysiology Pattern recognition Proteins Pyrin protein Sepsis Therapeutic targets |
| title | NLRP3 inflammasome in sepsis (Review) |
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