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  1 / 3190 MEDLINE  
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[PMID]:29465571
[Au] Autor:Wang YC; Liu QX; Liu T; Xu XE; Gao W; Bai XJ; Li ZF
[Ad] Endereço:Department of Traumatic Surgery, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, P.R. China.
[Ti] Título:Caspase-1-dependent pyroptosis of peripheral blood mononuclear cells predicts the development of sepsis in severe trauma patients: A prospective observational study.
[So] Source:Medicine (Baltimore);97(8):e9859, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pyroptosis plays a pivotal role in sepsis and septic shock in animal studies. However, its clinical significance in pathological conditions has not been well elucidated. This study aimed to evaluate the correlation between the percentage of pyroptotic peripheral blood mononuclear cells (PBMCs) and the clinical index and to investigate the relationship between PBMCs pyroptosis and the development of sepsis in trauma patients.This prospective study was conducted from October 2016 to May 2017 in a comprehensive trauma center. Sixty trauma patients and 10 healthy controls were enrolled. Peripheral blood samples were collected from the patients within 24 hours after injury. The percentages of pyroptotic and apoptotic PBMCs were measured using flow cytometry, and plasma levels of cytokines were evaluated using flow cytometric analysis with a human inflammation 13-plex panel.Trauma patients who developed sepsis had higher percentages of pyroptotic and apoptotic PBMCs at admission. Patients who developed sepsis (n = 33) had higher interleukin (IL)-6, IL-18, and monocyte chemotactic protein-1 (MCP-1) concentrations at admission than patients (n = 27) who did not develop sepsis. The percentage of PBMCs pyroptosis was significantly correlated with injury severity score (ISS), acute physiology and chronic health evaluation (APACHE) II score, IL-10, IL-18, and MCP-1 levels in trauma patients. PBMCs pyroptosis is a better biomarker in predicting the development of sepsis after trauma.This study indicates that the percentage of pyroptotic PBMCs increases during the early phase of trauma and that this increase is significantly correlated with the severity and state of inflammation in trauma patients. PBMCs pyroptosis is a potential marker for predicting the development of sepsis after trauma.
[Mh] Termos MeSH primário: Caspase 1/metabolismo
Leucócitos Mononucleares/citologia
Piroptose/fisiologia
Sepse/sangue
Sepse/etiologia
Ferimentos e Lesões/complicações
[Mh] Termos MeSH secundário: Adulto
Citocinas/sangue
Feminino
Seres Humanos
Escala de Gravidade do Ferimento
Leucócitos Mononucleares/enzimologia
Masculino
Meia-Idade
Estudos Prospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Cytokines); EC 3.4.22.36 (Caspase 1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180222
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009859


  2 / 3190 MEDLINE  
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[PMID]:28452921
[Au] Autor:Noda K; Tane S; Haam SJ; D'Cunha J; Hayanga AJ; Luketich JD; Shigemura N
[Ad] Endereço:Department of Cardiothoracic Surgery, University of Pittsburgh Medical Center, Pittsburgh, PA.
[Ti] Título:Targeting Circulating Leukocytes and Pyroptosis During Ex Vivo Lung Perfusion Improves Lung Preservation.
[So] Source:Transplantation;101(12):2841-2849, 2017 12.
[Is] ISSN:1534-6080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The role of the circulating leukocytes in lungs and their relationship with circulating proinflammatory cytokines during ischemia-reperfusion injury is not well understood. Using ex vivo lung perfusion (EVLP) to investigate the pathophysiology of isolated lungs, we aimed to identify a therapeutic target to optimize lung preservation leading to successful lung transplantation. METHODS: Rat heart-lung blocks were placed on EVLP for 4 hours with or without a leukocyte-depleting filter (LF). After EVLP, lung grafts were transplanted, and posttransplant outcomes were compared. RESULTS: Lung function was significantly better in lung grafts on EVLP with a LF than in lungs on EVLP without a LF. The interleukin (IL)-6 levels in the lung grafts and EVLP perfusate were also significantly lower after EVLP with a LF. Interestingly, IL-6 levels in the perfusate did not increase after the lungs were removed from the EVLP circuit, indicating that the cells trapped by the LF were not secreting IL-6. The trapped cells were analyzed with flow cytometry to detect apoptosis and pyroptosis; 26% were pyroptotic (Caspase-1-positive). After transplantation, there was better graft function and less inflammatory response if a LF was used or a caspase-1 inhibitor was administered during EVLP. CONCLUSIONS: Our data demonstrated that circulating leukocytes derived from donor lungs, and not circulating proinflammatory cytokines substantially impaired the quality of lung grafts through caspase-1-induced pyroptotic cell death during EVLP. Removing these cells with a LF and/or inhibiting pyroptosis of the cells can be a new therapeutic approach leading to long-term success after lung transplantation.
[Mh] Termos MeSH primário: Leucócitos/citologia
Transplante de Pulmão/métodos
Pulmão/patologia
Pulmão/fisiologia
Preservação de Órgãos/métodos
Piroptose
[Mh] Termos MeSH secundário: Animais
Ponte Cardiopulmonar
Caspase 1/metabolismo
Citocinas/metabolismo
Seres Humanos
Inflamação
Interleucina-6/metabolismo
Leucócitos/metabolismo
Masculino
Microcirculação
Perfusão
Ratos
Ratos Endogâmicos Lew
Testes de Função Respiratória
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Interleukin-6); EC 3.4.22.36 (Caspase 1)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1097/TP.0000000000001798


  3 / 3190 MEDLINE  
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[PMID]:29250536
[Au] Autor:Wang H; Zhou X; Li H; Qian X; Wang Y; Ma L
[Ad] Endereço:Department of Anesthesiology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou 310016, China.
[Ti] Título:Transient Receptor Potential Melastatin 2 Negatively Regulates LPS-ATP-Induced Caspase-1-Dependent Pyroptosis of Bone Marrow-Derived Macrophage by Modulating ROS Production.
[So] Source:Biomed Res Int;2017:2975648, 2017.
[Is] ISSN:2314-6141
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Pyroptosis, a new form of cell death, which has special morphological characteristics, depends on caspase-1 activation and occupies an important role in inflammatory immune diseases and ischemia-reperfusion injury. ROS is a common activator of NLR/caspase-1. Transient receptor potential melastatin 2 (TRPM2), a selective cation channel, is involved in inflammatory regulation. This study was designed to explore the role of TRPM2 in activating caspase-1 and caspase-1-dependent pyroptosis of mouse BMDMs. Methods: BMDMs isolated from WT and TRPM2-/- mice were treated with LPS and ATP, along with ROS inhibitor (NAC and DPI), caspase-1 inhibitor (Z-YVAD), or not. The activation of caspase-1 was measured by western blot. EtBr and EthD-2 staining were used to assess the incidence of pyroptosis. Results: Compared with WT, the activated caspase-1-P10 was higher and the percentage of EtBr positive cells was also increased in TRPM2-/- group, which were both inhibited by Z-YVAD, NAC, or DPI. ASC oligomerization was increased in TRPM2-/- group. Conclusion: Deletion of TRPM2 can enhance the activation of caspase-1 and pyroptosis, which may be via modulating ROS production, suggesting that TRPM2 plays a critical role in immune adjustment.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/metabolismo
Caspase 1/metabolismo
Macrófagos/metabolismo
Piroptose/fisiologia
Espécies Reativas de Oxigênio/metabolismo
Canais de Cátion TRPM/metabolismo
[Mh] Termos MeSH secundário: Animais
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Canais de Cátion TRPM/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 0 (TRPM Cation Channels); 0 (TRPM2 protein, mouse); 8L70Q75FXE (Adenosine Triphosphate); EC 3.4.22.36 (Caspase 1)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1155/2017/2975648


  4 / 3190 MEDLINE  
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[PMID]:27774630
[Au] Autor:Sun Q; Loughran P; Shapiro R; Shrivastava IH; Antoine DJ; Li T; Yan Z; Fan J; Billiar TR; Scott MJ
[Ad] Endereço:Department of Surgery, University of Pittsburgh, Pittsburgh, PA.
[Ti] Título:Redox-dependent regulation of hepatocyte absent in melanoma 2 inflammasome activation in sterile liver injury in mice.
[So] Source:Hepatology;65(1):253-268, 2017 01.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sterile liver inflammation, such as liver ischemia-reperfusion, hemorrhagic shock after trauma, and drug-induced liver injury, is initiated and regulated by endogenous mediators including DNA and reactive oxygen species. Here, we identify a mechanism for redox-mediated regulation of absent in melanoma 2 (AIM2) inflammasome activation in hepatocytes after redox stress in mice, which occurs through interaction with cytosolic high mobility group box 1 (HMGB1). We show that in liver during hemorrhagic shock in mice and in hepatocytes after hypoxia with reoxygenation, cytosolic HMGB1 associates with AIM2 and is required for activation of caspase-1 in response to cytosolic DNA. Activation of caspase-1 through AIM2 leads to subsequent hepatoprotective responses such as autophagy. HMGB1 binds to AIM2 at a non-DNA-binding site on the hematopoietic interferon-inducible nuclear antigen domain of AIM2 to facilitate inflammasome and caspase-1 activation in hepatocytes. Furthermore, binding of HMGB1 to AIM2 is stronger with fully reduced all-thiol HMGB1 than with partially oxidized disulfide-HMGB1, and binding strength corresponds to caspase-1 activation. These data suggest that HMGB1 redox status regulates AIM2 inflammasome activation. CONCLUSION: These findings suggest a novel and important mechanism for regulation of AIM2 inflammasome activation in hepatocytes during redox stress and may suggest broader implications for how this and other inflammasomes are activated and how their activation is regulated during cell stress, as well as the mechanisms of inflammasome regulation in nonimmune cell types. (Hepatology 2017;65:253-268).
[Mh] Termos MeSH primário: Proteínas de Ligação a DNA/fisiologia
Hepatócitos/metabolismo
Inflamassomos/metabolismo
Hepatopatias/etiologia
[Mh] Termos MeSH secundário: Animais
Caspase 1/metabolismo
Proteína HMGB1/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Oxirredução
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Aim2 protein, mouse); 0 (DNA-Binding Proteins); 0 (HMGB1 Protein); 0 (Inflammasomes); EC 3.4.22.36 (Caspase 1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180121
[Lr] Data última revisão:
180121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1002/hep.28893


  5 / 3190 MEDLINE  
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[PMID]:28465656
[Au] Autor:Yin Y; Chen F; Wang W; Wang H; Zhang X
[Ad] Endereço:Department of Ophthalmology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
[Ti] Título:Resolvin D1 inhibits inflammatory response in STZ-induced diabetic retinopathy rats: Possible involvement of NLRP3 inflammasome and NF-κB signaling pathway.
[So] Source:Mol Vis;23:242-250, 2017.
[Is] ISSN:1090-0535
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To investigate the effect of resolvin D1 (RvD1) on the Nod-like receptor family pyrin domain-containing (NLRP3) inflammasome and the nuclear factor-kappa beta (NF-κB) pathway in streptozotocin (STZ)-induced diabetic retinopathy in rats. METHODS: Ninety-six male rats were divided into four groups: control, STZ, RvD1, and vehicle. The rats with diabetic retinopathy induced by STZ in the RvD1 and vehicle groups were given an intravitreal injection of RvD1 (1,000 ng/kg) or the same dosage of vehicle, respectively. All rats were euthanized 7 days following treatment. Hematoxylin and eosin staining was used to observe the pathological changes in the retinal tissues. The location and expression of the NLRP3 inflammasome components, including NLRP3, caspase-associated recruitment domain (ASC), and caspase-1, in the retinas were detected using immunohistochemistry, real-time PCR, and western blot, respectively. Retinal homogenate of rats were collected for the detection of the downstream molecules interleukin 1 beta (IL-1ß) and IL-18 of the NLRP3 inflammasome with enzyme-linked immunosorbent assay kits. RESULTS: The levels of NLRP3, ASC, cleaved caspase-1, IL-1ß, and IL-18 were upregulated in the retinas of the STZ-induced diabetic rats; however, these changes were partially inhibited by the RvD1 treatment. Furthermore, the administration of RvD1 suppressed activation of NF-kB, which was upregulated in STZ-induced diabetic retinopathy. CONCLUSIONS: RvD1 plays a protective role in STZ-induced diabetic retinopathy by inhibiting the level of activation of the NLRP3 inflammasome and associated cytokine production, suggesting targeting of this pathway might be an effective strategy in treatment of diabetic retinopathy.
[Mh] Termos MeSH primário: Diabetes Mellitus Experimental/prevenção & controle
Retinopatia Diabética/prevenção & controle
Ácidos Docosa-Hexaenoicos/farmacologia
Inflamassomos/metabolismo
NF-kappa B/metabolismo
Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Caspase 1/metabolismo
Citocinas/metabolismo
Diabetes Mellitus Experimental/metabolismo
Retinopatia Diabética/metabolismo
Ensaio de Imunoadsorção Enzimática
Inflamassomos/genética
Inflamação/prevenção & controle
Injeções Intravítreas
Masculino
Proteína 3 que Contém Domínio de Pirina da Família NLR/genética
Ratos
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real
Estreptozocina
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Inflammasomes); 0 (NF-kappa B); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (Nlrp3 protein, rat); 0 (resolvin D1); 25167-62-8 (Docosahexaenoic Acids); 5W494URQ81 (Streptozocin); EC 3.4.22.36 (Caspase 1)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  6 / 3190 MEDLINE  
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[PMID]:29229137
[Au] Autor:Chang YY; Kao MC; Lin JA; Chen TY; Cheng CF; Wong CS; Tzeng IS; Huang CJ
[Ad] Endereço:Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan; Department of Anesthesiology, Taipei Tzu Chi Hospital, Taipei, Taiwan; School of Medicine, Tzu Chi University, Hualien, Taiwan.
[Ti] Título:Effects of MgSO on inhibiting Nod-like receptor protein 3 inflammasome involve decreasing intracellular calcium.
[So] Source:J Surg Res;221:257-265, 2018 Jan.
[Is] ISSN:1095-8673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Nod-like receptor protein 3 (NLRP3) inflammasome is a multiprotein complex composed of NLRP3, caspase-1, and apoptosis-associated speck-like protein containing a caspase recruitment domain. Activation of NLRP3 inflammasome leads to interleukin-1ß (IL-1ß) upregulation and pyroptosis, a proinflammatory cell death characterized by increased cell size. Of note, calcium signaling is crucial for NLRP3 inflammasome activation. This study elucidated the effects of magnesium sulfate (MgSO ), a potent calcium antagonist, on modulating NLRP3 inflammasome. MATERIALS AND METHODS: THP-1 cells, the human monocytic leukemia cell line, were treated with lipopolysaccharide (LPS, 1 µg/ml) plus nigericin (5 µM) (the LPS + Nig group) and LPS plus nigericin plus MgSO (20 mM) [the LPS + Nig + M(20)] to facilitate investigations. Levels of IL-1ß, pyroptosis, and NLRP3 inflammasome induction as well as intracellular calcium were assayed. RESULTS: IL-1ß concentration of the LPS + Nig + M(20) group was significantly lower than the LPS + Nig group (P = 0.001). Cell size of the LPS + Nig + M(20) group was significantly smaller than the LPS + Nig group (P < 0.001). Level of pyroptotic cell death of the LPS + Nig + M(20) group was significantly lower than the LPS + Nig group (P = 0.004). NLRP3 mRNA and protein concentrations of the LPS + Nig + M(20) group were also significantly lower than the LPS + Nig group (P = 0.021 and P < 0.001). Similarly, apoptosis-associated speck-like protein containing a caspase recruitment domain speck formation ratio and caspase-1 concentration of the LPS + Nig + M(20) group were significantly lower than the LPS + Nig group (both P < 0.001). The change in intracellular calcium level of the LPS + Nig + M(20) group was significantly smaller than the LPS + Nig group (P = 0.001). CONCLUSIONS: MgSO inhibits NLRP3 inflammasome, IL-1ß upregulation, and pyroptosis. The mechanism is consistent with decreased intracellular calcium levels.
[Mh] Termos MeSH primário: Sinalização do Cálcio/efeitos dos fármacos
Inflamassomos/antagonistas & inibidores
Sulfato de Magnésio/farmacologia
Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo
Piroptose/efeitos dos fármacos
[Mh] Termos MeSH secundário: Caspase 1/metabolismo
Domínio de Ativação e Recrutamento de Caspases
Seres Humanos
Interleucina-1beta/metabolismo
Células THP-1
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL1B protein, human); 0 (Inflammasomes); 0 (Interleukin-1beta); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (NLRP3 protein, human); 7487-88-9 (Magnesium Sulfate); EC 3.4.22.36 (Caspase 1)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE


  7 / 3190 MEDLINE  
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[PMID]:28459430
[Au] Autor:Wang Y; Gao W; Shi X; Ding J; Liu W; He H; Wang K; Shao F
[Ad] Endereço:College of Biological Sciences, China Agricultural University, Beijing 100094, China.
[Ti] Título:Chemotherapy drugs induce pyroptosis through caspase-3 cleavage of a gasdermin.
[So] Source:Nature;547(7661):99-103, 2017 07 06.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Pyroptosis is a form of cell death that is critical for immunity. It can be induced by the canonical caspase-1 inflammasomes or by activation of caspase-4, -5 and -11 by cytosolic lipopolysaccharide. The caspases cleave gasdermin D (GSDMD) in its middle linker to release autoinhibition on its gasdermin-N domain, which executes pyroptosis via its pore-forming activity. GSDMD belongs to a gasdermin family that shares the pore-forming domain. The functions and mechanisms of activation of other gasdermins are unknown. Here we show that GSDME, which was originally identified as DFNA5 (deafness, autosomal dominant 5), can switch caspase-3-mediated apoptosis induced by TNF or chemotherapy drugs to pyroptosis. GSDME was specifically cleaved by caspase-3 in its linker, generating a GSDME-N fragment that perforates membranes and thereby induces pyroptosis. After chemotherapy, cleavage of GSDME by caspase-3 induced pyroptosis in certain GSDME-expressing cancer cells. GSDME was silenced in most cancer cells but expressed in many normal tissues. Human primary cells exhibited GSDME-dependent pyroptosis upon activation of caspase-3 by chemotherapy drugs. Gsdme (also known as Dfna5 ) mice were protected from chemotherapy-induced tissue damage and weight loss. These findings suggest that caspase-3 activation can trigger necrosis by cleaving GSDME and offer new insights into cancer chemotherapy.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Caspase 3/metabolismo
Piroptose/efeitos dos fármacos
Receptores Estrogênicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Caspase 1/metabolismo
Linhagem Celular Tumoral
Seres Humanos
Lipopolissacarídeos/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
Fragmentos de Peptídeos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (DFNA5 protein, human); 0 (Dfna5h protein, mouse); 0 (Lipopolysaccharides); 0 (Peptide Fragments); 0 (Receptors, Estrogen); EC 3.4.22.- (Caspase 3); EC 3.4.22.36 (Caspase 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1038/nature22393


  8 / 3190 MEDLINE  
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[PMID]:28972095
[Au] Autor:Sadatomo A; Inoue Y; Ito H; Karasawa T; Kimura H; Watanabe S; Mizushina Y; Nakamura J; Kamata R; Kasahara T; Horie H; Sata N; Takahashi M
[Ad] Endereço:Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Tochigi 329-0498, Japan; and.
[Ti] Título:Interaction of Neutrophils with Macrophages Promotes IL-1ß Maturation and Contributes to Hepatic Ischemia-Reperfusion Injury.
[So] Source:J Immunol;199(9):3306-3315, 2017 Nov 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Accumulating evidence suggests that IL-1ß plays a pivotal role in the pathophysiology of hepatic ischemia-reperfusion (I/R) injury; however, the mechanism by which I/R triggers IL-1ß production in the liver remains unclear. Recent data have shown that neutrophils contribute to hepatic I/R injury independently of the inflammasomes regulating IL-1ß maturation. Thus, we investigated the role of neutrophils in IL-1ß maturation and tissue injury in a murine model of hepatic I/R. IL-1ß was released from the I/R liver and its deficiency reduced reactive oxygen species generation, apoptosis, and inflammatory responses, such as inflammatory cell infiltration and cytokine expression, thereby resulting in reduced tissue injury. Depletion of either macrophages or neutrophils also attenuated IL-1ß release and hepatic I/R injury. In vitro experiments revealed that neutrophil-derived proteinases process pro-IL-1ß derived from macrophages into its mature form independently of caspase-1. Furthermore, pharmacological inhibition of serine proteases attenuated IL-1ß release and hepatic I/R injury in vivo. Taken together, the interaction between neutrophils and macrophages promotes IL-1ß maturation and causes IL-1ß-driven inflammation in the I/R liver. Both neutrophils and macrophages are indispensable in this process. These findings suggest that neutrophil-macrophage interaction is a therapeutic target for hepatic I/R injury and may also provide new insights into the inflammasome-independent mechanism of IL-1ß maturation in the liver.
[Mh] Termos MeSH primário: Comunicação Celular/imunologia
Interleucina-1beta/imunologia
Hepatopatias/imunologia
Fígado/imunologia
Macrófagos/imunologia
Neutrófilos/imunologia
Traumatismo por Reperfusão/imunologia
[Mh] Termos MeSH secundário: Animais
Caspase 1/genética
Caspase 1/imunologia
Comunicação Celular/genética
Interleucina-1beta/genética
Fígado/patologia
Hepatopatias/genética
Hepatopatias/patologia
Macrófagos/patologia
Camundongos
Camundongos Knockout
Neutrófilos/patologia
Traumatismo por Reperfusão/genética
Traumatismo por Reperfusão/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL1B protein, mouse); 0 (Interleukin-1beta); EC 3.4.22.36 (Caspase 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700717


  9 / 3190 MEDLINE  
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[PMID]:28961278
[Au] Autor:McClellan SA; Jerome A; Suvas S; Hazlett LD
[Ad] Endereço:Department of Anatomy and Cell Biology, Wayne State University School of Medicine, Detroit, MI, United States of America.
[Ti] Título:NLRC4 regulates caspase-1 and IL-1beta production in a CD11blowLy6Glow population of cells required for resistance to Pseudomonas aeruginosa keratitis.
[So] Source:PLoS One;12(9):e0185718, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Psbetaeudomonas (P.) aeruginosa infection of the cornea in BALB/c mice does not result in perforation and the mice have been classified as resistant. However, regulation of this response via inflammasome activation remained untested. Therefore, BALB/c mice were infected with P. aeruginosa ATCC strain 19660 and NLRP3 and NLRC4 protein tested by ELISA. Since NLRC4 vs NLRP3 protein levels were significantly higher in the corneas of BALB/c at 1 and 5 days postinfection we used silencing to knockdown NLRC4. Silencing NLRC4 vs scrambled siRNA treatment exacerbated disease in BALB/c mice, reduced myeloperoxidase levels and elevated bacterial plate counts at 5 days postinfection. It also increased pro IL-1beta, but reduced total protein for IL-1beta and IL-18 at 5 days postinfection. Flow cytometry to identify cells affected by silencing, showed reduced caspase-1 levels in a CD11blowLy6Glow population of cells, (but not PMN or macrophages) from the infected cornea of siNLRC4 treated mice that produced less mature IL-1beta. These data provide evidence that the NLRC4 inflammasome contributes to resistance through regulation of caspase-1, IL-1beta and IL-18 in a CD11blowLy6Glow population of cells.
[Mh] Termos MeSH primário: Proteínas Reguladoras de Apoptose/fisiologia
Antígeno CD11b/imunologia
Proteínas de Ligação ao Cálcio/fisiologia
Caspase 1/biossíntese
Interleucina-1beta/biossíntese
Ceratite/imunologia
Infecções por Pseudomonas/imunologia
Pseudomonas aeruginosa/isolamento & purificação
[Mh] Termos MeSH secundário: Animais
Proteínas Reguladoras de Apoptose/genética
Proteínas de Ligação ao Cálcio/genética
Contagem de Colônia Microbiana
Ensaio de Imunoadsorção Enzimática
Feminino
Citometria de Fluxo
Técnicas de Silenciamento de Genes
Ceratite/microbiologia
Camundongos
Camundongos Endogâmicos BALB C
Infecções por Pseudomonas/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (CD11b Antigen); 0 (Calcium-Binding Proteins); 0 (Interleukin-1beta); 0 (Ipaf protein, mouse); EC 3.4.22.36 (Caspase 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170930
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185718


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[PMID]:28912259
[Au] Autor:Tschöpe C; Müller I; Xia Y; Savvatis K; Pappritz K; Pinkert S; Lassner D; Heimesaat MM; Spillmann F; Miteva K; Bereswill S; Schultheiss HP; Fechner H; Pieske B; Kühl U; Van Linthout S
[Ad] Endereço:From the Department of Cardiology and Pneumology, Charité-Universitätsmedizin Berlin, Campus Virchow Klinikum, Germany (C.T., Y.X., K.S., F.S., B.P., U.K., S.V.L.); DZHK (German Center for Cardiovascular Research), partner site Berlin, Germany (C.T., I.M., K.P., B.P., S.V.L.); Berlin-Brandenburg Cen
[Ti] Título:NOD2 (Nucleotide-Binding Oligomerization Domain 2) Is a Major Pathogenic Mediator of Coxsackievirus B3-Induced Myocarditis.
[So] Source:Circ Heart Fail;10(9), 2017 Sep.
[Is] ISSN:1941-3297
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The cytoplasmatic pattern recognition receptor, NOD2 (nucleotide-binding oligomerization domain 2), belongs to the innate immune system and is among others responsible for the recognition of single-stranded RNA. With Coxsackievirus B3 (CVB3) being a single-stranded RNA virus, and the recent evidence that the NOD2 target, NLRP3 (NOD-like receptor family, pyrin domain containing 3) is of importance in the pathogenesis of CVB3-induced myocarditis, we aimed to unravel the role of NOD2 in CVB3-induced myocarditis. METHODS AND RESULTS: Endomyocardial biopsy NOD2 mRNA expression was higher in CVB3-positive patients compared with patients with myocarditis but without evidence of persistent CVB3 infection. Left ventricular NOD2 mRNA expression was also induced in CVB3-induced myocarditis versus healthy control mice. NOD2 knockdown mice were rescued from the detrimental CVB3-mediated effects as shown by a reduced cardiac inflammation (less cardiac infiltrates and suppression of proinflammatory cytokines), cardiac fibrosis, apoptosis, lower CAR (Coxsackievirus and adenovirus receptor) expression and CVB3 copy number, and an improved left ventricular function in NOD2 CVB3 mice compared with wild-type CVB3 mice. In agreement, NOD2 decreased the CVB3-induced inflammatory response, CVB3 copy number, and apoptosis in vitro. NOD2 was further associated with a reduction in CVB3-induced NLRP3 expression and activity as evidenced by lower ASC (apoptosis-associated speck-like protein containing a CARD) expression, caspase 1 activity, or IL-1ß (interleukin-1ß) protein expression under in vivo and in vitro CVB3 conditions. CONCLUSIONS: NOD2 is an important mediator in the viral uptake and inflammatory response during the pathogenesis of CVB3 myocarditis.
[Mh] Termos MeSH primário: Infecções por Coxsackievirus/metabolismo
Enterovirus Humano B/metabolismo
Miocardite/metabolismo
Miocárdio/metabolismo
Proteína Adaptadora de Sinalização NOD2/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Proteínas Reguladoras de Apoptose/metabolismo
Proteínas Adaptadoras de Sinalização CARD
Estudos de Casos e Controles
Caspase 1/metabolismo
Linhagem Celular
Infecções por Coxsackievirus/imunologia
Infecções por Coxsackievirus/prevenção & controle
Infecções por Coxsackievirus/virologia
Modelos Animais de Doenças
Enterovirus Humano B/genética
Enterovirus Humano B/imunologia
Predisposição Genética para Doença
Interações Hospedeiro-Patógeno
Seres Humanos
Interleucina-1beta/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Miocardite/imunologia
Miocardite/prevenção & controle
Miocardite/virologia
Miocárdio/imunologia
Miocárdio/patologia
Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo
Proteína Adaptadora de Sinalização NOD2/deficiência
Proteína Adaptadora de Sinalização NOD2/genética
Fenótipo
Interferência de RNA
Transdução de Sinais
Transfecção
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (CARD Signaling Adaptor Proteins); 0 (Card15 protein, mouse); 0 (IL1B protein, mouse); 0 (Interleukin-1beta); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (NOD2 protein, human); 0 (Nlrp3 protein, mouse); 0 (Nod2 Signaling Adaptor Protein); 0 (Pycard protein, mouse); EC 3.4.22.36 (Caspase 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE



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