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Pesquisa : D12.644.276.374.200.120.100 [Categoria DeCS]
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[PMID]:29222050
[Au] Autor:Li N; Cao M; Yi S; Cheng J; Wang L; Tao Y; Wu D; Peng J; Zhang M; Qi P; Zhao J
[Ad] Endereço:Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu 610065, Sichuan, PR China.
[Ti] Título:Effects of the RNA-binding protein, KSRP, on innate immune response against Helicobacter pylori infection in mice.
[So] Source:Biochem Biophys Res Commun;495(2):1573-1579, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Helicobacter pylori (H. pylori) contributes to various gastric diseases such as chronic gastritis, gastric ulcer, and gastric carcinoma. Host innate immune response against the pathogen plays a significant role in elimination of pathogen infection. Importantly, pathogen elimination is closely related to numerous inflammatory-related genes that participate in complex biological response of cells to harmful stimuli. Here we studied effects of the KH-type splicing regulatory protein (KSRP), a RNA-binding protein, on innate immune response against H. pylori infection. We found that H. pylori infection downregulated KSRP expression directly, and that KSRP overexpression repressed upregulation of CXCL-2 expression induced by H. pylori and facilitated H. pylori proliferation in vitro. Similarly, KSRP overexpression in H. pylori mice also facilitated H. pylori proliferation and colonization, and induced more severe gastric mucosal damage. Intriguingly, CXCL-2 and HMOX-1 were upregulated in H. pylori infected mice after KSRP overexpression. This difference in expression of these genes implicated that KSRP was closely associated with and directly participated in the innate immune response against H. pylori. These results were beneficial for understanding the in vivo function of KSRP on innate immune response against pathogen infection.
[Mh] Termos MeSH primário: Infecções por Helicobacter/imunologia
Helicobacter pylori
Proteínas de Ligação a RNA/imunologia
Transativadores/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Quimiocina CXCL2/genética
Regulação para Baixo
Feminino
Gastrite/genética
Gastrite/imunologia
Gastrite/patologia
Infecções por Helicobacter/genética
Infecções por Helicobacter/patologia
Helicobacter pylori/genética
Helicobacter pylori/imunologia
Helicobacter pylori/patogenicidade
Heme Oxigenase-1/genética
Seres Humanos
Imunidade Inata/genética
Masculino
Proteínas de Membrana/genética
Camundongos
Camundongos Endogâmicos BALB C
Proteínas de Ligação a RNA/genética
Receptor 2 Toll-Like/genética
Transativadores/genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CXCL2 protein, human); 0 (Chemokine CXCL2); 0 (Cxcl2 protein, mouse); 0 (KHSRP protein, human); 0 (KSRP protein, mouse); 0 (Membrane Proteins); 0 (RNA-Binding Proteins); 0 (TLR2 protein, human); 0 (Tlr2 protein, mouse); 0 (Toll-Like Receptor 2); 0 (Trans-Activators); EC 1.14.14.18 (HMOX1 protein, human); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.14.14.18 (Hmox1 protein, mouse)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171210
[St] Status:MEDLINE


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[PMID]:28456769
[Au] Autor:Al Dera H
[Ad] Endereço:Department of Basic Medical Sciences, College of Medicine at King Saud bin Abdulaziz University for Health Sciences (KSAU-HS), Riyadh, Kingdom of Saudi Arabia. derah@ksau-hs.edu.sa.
[Ti] Título:Neuroprotective effect of resveratrol against late cerebral ischemia reperfusion induced oxidative stress damage involves upregulation of osteopontin and inhibition of interleukin-1beta.
[So] Source:J Physiol Pharmacol;68(1):47-56, 2017 Feb.
[Is] ISSN:1899-1505
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:This study was carried out to investigate the expression pattern and role of osteopontin (OPN) in late global ischemia-reperfusion (I/R) injury with or without resveratrol (RES) pre-treatment. Young male rats were divided into 3 groups (n = 12) of I) sham, II) I/R model group and III) I/R + RES. Vehicle and RES (20 mg/kg) were administered to designed groups intraperitoneally 30 days prior global I/R injury (2-VO) induction and continued for 7 days, later. Then, percentages of infarct areas, mRNA levels of OPN, inducible nitric oxide synthase (iNOS) and other biochemical parameter related to endogenous antioxidants activities and inflammation were measured in the cerebral cortices of all groups. Significant elevations in the levels of malondialdehyde (MDA), the inflammatory mediator interleukin 1ß (IL-1ß), chemokines (KC and MIP-2) and adhesive molecules (ICAM-1) as well as parallel reductions in enzymes activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and chloramphenicol acetyltransferase (CAT) were observed in the cerebral homogenates of rats with late I/R injury. Associated with these changes, mRNA levels of OPN were significantly downregulated and those of iNOS and Bax were upregulated. All these changes were reversed by in 2-VO I/R induced rats pre-administered RES. These findings suggest that inhibition of sustained inflammatory response driven by IL-1ß, decreased activities of endogenous antioxidants and downregulation of OPN induced upregulation of iNOS play important roles in the pathogenesis of neurodegeneration during late cerebral I/R injury, effects that can be modulated by RES which might explain its neuroprotection effect during late global ischemia.
[Mh] Termos MeSH primário: Isquemia Encefálica/metabolismo
Fármacos Neuroprotetores/farmacologia
Traumatismo por Reperfusão/metabolismo
Estilbenos/farmacologia
[Mh] Termos MeSH secundário: Animais
Isquemia Encefálica/tratamento farmacológico
Catalase/metabolismo
Córtex Cerebral/metabolismo
Quimiocina CXCL2/metabolismo
Quimiocinas/metabolismo
Glutationa Peroxidase/metabolismo
Molécula 1 de Adesão Intercelular/metabolismo
Interleucina-1beta/antagonistas & inibidores
Interleucina-1beta/metabolismo
Masculino
Fármacos Neuroprotetores/uso terapêutico
Óxido Nítrico Sintase Tipo II/genética
Osteopontina/genética
Estresse Oxidativo/efeitos dos fármacos
Ratos Wistar
Traumatismo por Reperfusão/tratamento farmacológico
Estilbenos/uso terapêutico
Superóxido Dismutase/metabolismo
Regulação para Cima
Proteína X Associada a bcl-2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bax protein, rat); 0 (Chemokine CXCL2); 0 (Chemokines); 0 (Cxcl2 protein, rat); 0 (IL1B protein, rat); 0 (Interleukin-1beta); 0 (Neuroprotective Agents); 0 (Spp1 protein, rat); 0 (Stilbenes); 0 (bcl-2-Associated X Protein); 106441-73-0 (Osteopontin); 126547-89-5 (Intercellular Adhesion Molecule-1); 147037-79-4 (keratinocyte-derived chemokines); EC 1.11.1.6 (Catalase); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, rat); EC 1.15.1.1 (Superoxide Dismutase); Q369O8926L (resveratrol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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[PMID]:28463395
[Au] Autor:de la Varga Martínez R; Rodríguez-Bayona B; Añez GA; Medina Varo F; Pérez Venegas JJ; Brieva JA; Rodríguez C
[Ad] Endereço:Unidad de Investigación, Hospital Universitario Puerta del Mar (HUPM), Cádiz.
[Ti] Título:Clinical relevance of circulating anti-ENA and anti-dsDNA secreting cells from SLE patients and their dependence on STAT-3 activation.
[So] Source:Eur J Immunol;47(7):1211-1219, 2017 07.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Disturbances of plasma cell homeostasis and auto-antibody production are hallmarks of systemic lupus erythematosus. The aim of this study was to explore the presence of circulating anti-ENA and anti-dsDNA antibody-secreting cells, to determine their dependence on plasma cell-niche cytokines and to analyze their clinical value. The study was performed in SLE patients with serum anti-ENA and/or anti-dsDNA antibodies (n = 57). Enriched B-cell fractions and sorted antibody-secreting cells (CD19 CD38 ) were obtained from blood. dsDNA- and ENA-specific antibody-secreting cells were identified as cells capable of active auto-antibody production in culture. The addition of a combination of IL-6, IL-21, BAFF, APRIL, and CXCL12 to the cultures significantly augmented auto-antibody production and antibody-secreting cell proliferation, whereas it diminished apoptosis. The effect on auto-antibody production was dependent on STAT-3 activation as it was abrogated in the presence of the JAK/STAT-3 pathway inhibitors ruxolitinib and stattic. Among patients with serum anti-dsDNA antibodies, the detection of circulating anti-dsDNA-antibody-secreting cells was associated with higher disease activity markers. In conclusion, auto-antibody production in response to plasma cell-niche cytokines that are usually at high levels in SLE patients is dependent on JAK/STAT-3 activation. Thus, patients with circulating anti-dsDNA antibody-secreting cells and active disease could potentially benefit from therapies targeting the JAK/STAT3 pathway.
[Mh] Termos MeSH primário: Anticorpos Antinucleares/sangue
Células Produtoras de Anticorpos/imunologia
DNA/imunologia
Lúpus Eritematoso Sistêmico/imunologia
Fator de Transcrição STAT3/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Anticorpos Antinucleares/imunologia
Células Produtoras de Anticorpos/efeitos dos fármacos
Apoptose/efeitos dos fármacos
Fator Ativador de Células B/farmacologia
Proliferação Celular
Quimiocina CXCL2/farmacologia
Óxidos S-Cíclicos/farmacologia
DNA/sangue
Feminino
Seres Humanos
Interleucina-6/farmacologia
Interleucinas/farmacologia
Lúpus Eritematoso Sistêmico/sangue
Masculino
Meia-Idade
Pirazóis/farmacologia
Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/farmacologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Antinuclear); 0 (B-Cell Activating Factor); 0 (CXCL2 protein, human); 0 (Chemokine CXCL2); 0 (Cyclic S-Oxides); 0 (INCB018424); 0 (Interleukin-6); 0 (Interleukins); 0 (Pyrazoles); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 0 (TNFSF13B protein, human); 0 (Tumor Necrosis Factor Ligand Superfamily Member 13); 0 (interleukin-21); 0 (stattic); 9007-49-2 (DNA)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171202
[Lr] Data última revisão:
171202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201646872


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[PMID]:28846693
[Au] Autor:Wang H; Qu Y; Dai B; Zhu Y; Shi G; Zhu Y; Shen Y; Zhang H; Ye D
[Ad] Endereço:Department of Urology, Shanghai Cancer Center, Fudan University, Shanghai, China.
[Ti] Título:PBRM1 regulates proliferation and the cell cycle in renal cell carcinoma through a chemokine/chemokine receptor interaction pathway.
[So] Source:PLoS One;12(8):e0180862, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PBRM1 is a novel tumor suppressor gene that can inhibit cancer cell proliferation and predict the outcome of renal cell carcinoma (RCC), but its biological role needs further elucidation. We examined expression of the PBRM1 gene in RCC cell lines and the effect of PBRM1 on cell proliferation and cell cycle in RCC ACHN cells. Microarray processing and analysis was used to explore novel pathways involved in tumorigenesis related to PBRM1 knockdown. PBRM1 was expressed at high levels in RCC ACHN cells and lentivirus-mediated PBRM1 knockdown in these cells caused an increase in the proportion of cells in S phase of the cell cycle and promoted in vitro proliferation and migration. In vivo experiments showed that downregulation of PBRM1 promoted tumorigenesis in nude mice. In pathway gene chip analysis, the chemokine/chemokine receptor interaction pathway showed the greatest difference in gene expression upon PBRM1 knockdown. Protein levels of IL6ST and CCL2 were increased, whereas levels of interleukin (IL)-8, IL-6, and CXCL2 were decreased, in knockdown cells. Re-expression of IL-8 in PBRM1 knockdown ACHN cells could significantly decrease cell proliferation/migration and induced cell arrest in the G2/M phase. These findings indicate that PBRM1 alters cell cycle progression and inhibits proliferation and migration of ACHN cells through the chemokine/chemokine receptor pathway.
[Mh] Termos MeSH primário: Carcinoma de Células Renais/metabolismo
Ciclo Celular/fisiologia
Proliferação Celular/fisiologia
Quimiocinas/metabolismo
Proteínas HMGB/metabolismo
Neoplasias Renais/metabolismo
Receptores de Quimiocinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Carcinogênese/genética
Carcinoma de Células Renais/patologia
Linhagem Celular Tumoral
Movimento Celular/fisiologia
Quimiocina CCL2/genética
Quimiocina CCL2/metabolismo
Quimiocina CXCL2/genética
Quimiocina CXCL2/metabolismo
Regulação para Baixo
Regulação Neoplásica da Expressão Gênica
Técnicas de Silenciamento de Genes
Proteínas HMGB/genética
Seres Humanos
Interleucina-6/genética
Interleucina-6/metabolismo
Interleucina-8/genética
Interleucina-8/metabolismo
Neoplasias Renais/patologia
Camundongos
Camundongos Nus
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CCL2); 0 (Chemokine CXCL2); 0 (Chemokines); 0 (HMGB Proteins); 0 (Interleukin-6); 0 (Interleukin-8); 0 (Pbrm1 protein, mouse); 0 (Receptors, Chemokine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180862


  5 / 1609 MEDLINE  
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[PMID]:28813446
[Au] Autor:Rentzsch I; Santos CL; Huhle R; Ferreira JMC; Koch T; Schnabel C; Koch E; Pelosi P; Rocco PRM; Gama de Abreu M
[Ad] Endereço:Department of Anesthesiology and Intensive Care Therapy, Pulmonary Engineering Group, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
[Ti] Título:Variable stretch reduces the pro-inflammatory response of alveolar epithelial cells.
[So] Source:PLoS One;12(8):e0182369, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mechanical ventilation has the potential to increase inflammation in both healthy and injured lungs. Several animal studies have shown that variable ventilation recruits the lungs and reduces inflammation. However, it is unclear which cellular mechanisms are involved in those findings. We hypothesized that variable stretch of LPS-stimulated alveolar epithelial cells (AECs) reduces the production of pro-inflammatory cytokines compared to non-variable stretch. AECs were subjected to non-variable or variable cyclic stretch (sinusoidal pattern), with and without LPS stimulation. The expression and release of interleukin-6, CXCL-2 and CCL-2 mRNA were analyzed after 4 hours. The phosphorylation of the MAPKs ERK1/2 and SAPK/JNK was determined by Western Blot analysis at 0, 15, 30, 45 and 60 min of cyclic stretch. In LPS-stimulated AECs, variable cyclic cell stretching led to reduced cytokine expression and release compared to non-variable cell stretching. Furthermore, the phosphorylation of the MAPK ERK1/2 was increased after 30 minutes in non-variable stretched AECs, whereas variable stretched cells demonstrated only the non-stretched level of phosphorylation. After the 4h period of cyclic cell stretch and inhibition of the ERK1/2, but not the SAPK/JNK, signaling pathway, the gene expression of investigated cytokines increased in variable stretched, and decreased in non-variable stretched AECs. We conclude that in LPS-stimulated AECs, variable stretch reduced the pro-inflammatory response compared to non-variable stretch. This effect was mediated by the ERK1/2 signaling pathway, and might partly explain the findings of reduced lung inflammation during mechanical ventilation modes that enhance breath-by-breath variability of the respiratory pattern.
[Mh] Termos MeSH primário: Células Epiteliais Alveolares/fisiologia
[Mh] Termos MeSH secundário: Células Epiteliais Alveolares/efeitos dos fármacos
Células Epiteliais Alveolares/enzimologia
Animais
Western Blotting
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/fisiologia
Quimiocina CXCL2/metabolismo
Interleucina-6/metabolismo
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Lipopolissacarídeos/farmacologia
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Fosforilação
Alvéolos Pulmonares/metabolismo
Ratos
Transdução de Sinais/fisiologia
Junções Íntimas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL2); 0 (Interleukin-6); 0 (Lipopolysaccharides); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170817
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182369


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[PMID]:28739876
[Au] Autor:Boro M; Balaji KN
[Ad] Endereço:Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore 560012, India.
[Ti] Título:CXCL1 and CXCL2 Regulate NLRP3 Inflammasome Activation via G-Protein-Coupled Receptor CXCR2.
[So] Source:J Immunol;199(5):1660-1671, 2017 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammation is an extensively concerted process that confers protection to the host encountering immune insult. The major inflammatory mediators include IL-1 family members, such as IL-1ß, and the functional activation of such molecules is arbitrated by their regulated cleavage brought about by components of a multiprotein complex called inflammasome. In this context, NLR family pyrin domain containing 3 (NLRP3) inflammasome activation often acts as a rate-limiting step in regulating critical cell-fate decisions in various inflammatory scenarios. In this study, we identify the G-protein-coupled receptor CXCR2 (recognizing chemokines CXCL1 and CXCL2) as another arm feeding into the regulated activation of NLRP3 inflammasome in macrophages. We demonstrate that in vivo blocking of CXCL1 and CXCL2 can significantly reduce the -induced bioactive IL-1ß production. Further, CXCL1 could amplify the inflammasome activation in in vivo mouse models of carrageenan-induced inflammation in footpads and air pouches. The mechanistic insights revealed CXCR2-driven protein kinase C µ-dependent integrin-linked kinase to be essential for CXCL1-mediated activation of NLRP3 inflammasome. Blocking the activity of integrin-linked kinase or protein kinase C µ either by small interfering RNA-mediated knockdown or pharmacological inhibitor compromised inflammasome activation and subsequent production of bioactive IL-1ß. Taken together, our study demonstrates CXCR2-driven activation of NLRP3 inflammasome in macrophages and indicates a potential host-directed therapeutic target to limit the damaging inflammation associated with overt production of proinflammatory IL-1ß.
[Mh] Termos MeSH primário: Inflamassomos/metabolismo
Macrófagos/imunologia
Mycobacterium tuberculosis/imunologia
Receptores Acoplados a Proteínas-G/metabolismo
Receptores de Interleucina-8B/metabolismo
Tuberculose/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Neutralizantes/administração & dosagem
Células Cultivadas
Quimiocina CXCL1/imunologia
Quimiocina CXCL1/metabolismo
Quimiocina CXCL2/imunologia
Quimiocina CXCL2/metabolismo
Seres Humanos
Interleucina-1beta/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Proteína 3 que Contém Domínio de Pirina da Família NLR/genética
Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo
RNA Interferente Pequeno/genética
Receptores Acoplados a Proteínas-G/imunologia
Receptores de Interleucina-8B/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (Chemokine CXCL1); 0 (Chemokine CXCL2); 0 (Cxcl1 protein, mouse); 0 (Cxcl2 protein, mouse); 0 (Inflammasomes); 0 (Interleukin-1beta); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (Nlrp3 protein, mouse); 0 (RNA, Small Interfering); 0 (Receptors, G-Protein-Coupled); 0 (Receptors, Interleukin-8B)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700129


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[PMID]:28662496
[Au] Autor:Chaochao Q; Lou G; Yang Y; Liu Y; Hu Y; Min Z; Chen P; He J; Chen Z
[Ad] Endereço:State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Hangzhou, China.
[Ti] Título:Macrophage Inflammatory Protein-2 in High Mobility Group Box 1 Secretion of Macrophage Cells Exposed to Lipopolysaccharide.
[So] Source:Cell Physiol Biochem;42(3):913-928, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Macrophage inflammatory protein-2 (MIP-2), a type of leukocyte chemokine, is primarily produced by macrophages, and levels increase significantly in early inflammation. However, the precise biological functions and mechanisms of MIP-2 in the development of inflammation remain unclear. The purposes of the present study were to investigate the role of MIP-2 in inflammation induced by lipopolysaccharide (LPS) in vitro and to determine the possibility of blocking the high mobility group box 1 (HMGB1) signalling pathway via MIP-2 inhibition. METHODS: Macrophage cells (RAW264.7, U937 and THP-1 cells) were divided into control and treatments groups. Expression levels of interleukin-6 (IL-6), interleukin-1ß (IL-1ß), tumour necrosis factor-α (TNF-α), HMGB1, chemokine (C-C motif) ligand-2 (Ccl-2), Toll-like receptor-4 (TLR-4), inducible nitric oxide synthase (iNOS), phosphorylated MAPKs (p38, ERKs, JNKs), PI3K/Akts, JAKs/STAT3, IκB, and cytoplasmic and nuclear NF-κB p65 in RAW264.7 cells were detected by qRT-PCR, enzyme-linked immunosorbent assay (ELISA) or western blot assays. RESULTS: mip-2 siRNA and an anti-MIP-2 antibody significantly reduced the expression levels of Ccl-2, TLR-4, iNOS, IL-6, IL-1ß, HMGB1, and TNF-α in RAW264.7 cells exposed to LPS (P<0.01). Additionally, mRNA expression levels of HMGB1 and TLR-4 in cells treated with LPS+mip-2 siRNA were significantly lower than those in cells treated with LPS alone (P<0.01 or P<0.05). The MIP-2 antibody significantly suppressed activation of p38-MAPK, p-STAT3, and p-Akts and translocation of NF-κB p65 from the cytoplasm to the nucleus in RAW264.7 exposed to LPS (P<0.01 or P<0.05). CONCLUSION: mip-2 siRNA and the MIP-2 antibody can reduce the inflammatory effects induced by LPS in macrophage cells. The mechanisms may occur through down-regulation of p38-MAPK, STAT3 and Akts phosphorylation and translocation of NF-κB p65. MIP-2 plays an important role in inflammation induced by LPS.
[Mh] Termos MeSH primário: Quimiocina CXCL2/imunologia
Proteína HMGB1/imunologia
Inflamação/imunologia
Lipopolissacarídeos/imunologia
Macrófagos/imunologia
Interferência de RNA
[Mh] Termos MeSH secundário: Animais
Quimiocina CXCL2/genética
Regulação para Baixo
Regulação da Expressão Gênica
Proteína HMGB1/genética
Inflamação/genética
Interleucina-1beta/genética
Interleucina-6/genética
Macrófagos/metabolismo
Camundongos
Óxido Nítrico Sintase Tipo II/genética
Células RAW 264.7
RNA Interferente Pequeno/genética
Receptor 4 Toll-Like/genética
Fator de Necrose Tumoral alfa/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL2); 0 (HMGB1 Protein); 0 (HMGB1 protein, mouse); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Lipopolysaccharides); 0 (RNA, Small Interfering); 0 (Toll-Like Receptor 4); 0 (Tumor Necrosis Factor-alpha); EC 1.14.13.39 (Nitric Oxide Synthase Type II)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170630
[St] Status:MEDLINE
[do] DOI:10.1159/000478646


  8 / 1609 MEDLINE  
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[PMID]:28584076
[Au] Autor:Rajasagi NK; Bhela S; Varanasi SK; Rouse BT
[Ad] Endereço:Biomedical and Diagnostic Sciences, College of Veterinary Medicine, The University of Tennessee, Knoxville, Tennessee, USA; and nrajasag@utk.edu.
[Ti] Título:Frontline Science: Aspirin-triggered resolvin D1 controls herpes simplex virus-induced corneal immunopathology.
[So] Source:J Leukoc Biol;102(5):1159-1171, 2017 Nov.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Stromal keratitis (SK) is a chronic immunopathological lesion of the eye, caused by HSV-1 infection, and a common cause of vision impairment in humans. The inflammatory lesions in the cornea are primarily caused by neutrophils with the active participation of CD4 T cells. Therefore, the targeting of these immune cell types and their products represents a potentially valuable form of therapy to reduce the severity of disease. Resolvin D1 (RvD1) and its epimer aspirin-triggered RvD1 (AT-RvD1) are lipid mediators derived from docosahexaenoic acid (DHA) and were shown to promote resolution in several inflammatory disease models. In this report, we examined whether AT-RvD1 administration, begun before infection or at a later stage after ocular infection of mice with HSV-1, could control the severity of SK lesions. Treatment with AT-RvD1 significantly diminished the extent of corneal neovascularization and the severity of SK lesions. AT-RvD1-treated mice had fewer numbers of inflammatory cells that included neutrophils as well as Th1 and Th17 cells in the infected cornea. The mechanisms by which AT-RvD1 acts appear to be multiple. These include inhibitory effects on proinflammatory mediators, such as IL-1ß, IL-6, IL-12, CXCL1, MCP-1, MIP-2, vascular endothelial growth factor (VEGF)-A, matrix metalloproteinase 9 (MMP-9), and proinflammatory miRNA, such as miR-155, miR-132, and miR-223, which are involved in SK pathogenesis and corneal neovascularization. In addition, AT-RvD1 attenuated STAT1, which plays an important role in Th1 cell differentiation and IFN-γ expression. These findings demonstrate that AT-RvD1 treatment could represent a useful strategy for the management of virus-induced immunopathological lesions.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/farmacologia
Antivirais/farmacologia
Aspirina/farmacologia
Neovascularização da Córnea/tratamento farmacológico
Ácidos Docosa-Hexaenoicos/farmacologia
Herpes Simples/tratamento farmacológico
Ceratite Herpética/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Aspirina/análogos & derivados
Quimiocina CCL2/antagonistas & inibidores
Quimiocina CCL2/genética
Quimiocina CCL2/imunologia
Quimiocina CXCL2/antagonistas & inibidores
Quimiocina CXCL2/genética
Quimiocina CXCL2/imunologia
Neovascularização da Córnea/genética
Neovascularização da Córnea/imunologia
Neovascularização da Córnea/virologia
Substância Própria/irrigação sanguínea
Substância Própria/efeitos dos fármacos
Substância Própria/patologia
Substância Própria/virologia
Feminino
Regulação da Expressão Gênica
Herpes Simples/genética
Herpes Simples/imunologia
Herpes Simples/virologia
Herpesvirus Humano 1/efeitos dos fármacos
Herpesvirus Humano 1/crescimento & desenvolvimento
Herpesvirus Humano 1/patogenicidade
Seres Humanos
Interleucinas/antagonistas & inibidores
Interleucinas/genética
Interleucinas/imunologia
Ceratite Herpética/genética
Ceratite Herpética/imunologia
Ceratite Herpética/virologia
Metaloproteinase 9 da Matriz/genética
Metaloproteinase 9 da Matriz/imunologia
Camundongos
Camundongos Endogâmicos BALB C
MicroRNAs/antagonistas & inibidores
MicroRNAs/genética
MicroRNAs/imunologia
Neutrófilos/efeitos dos fármacos
Neutrófilos/imunologia
Neutrófilos/virologia
Índice de Gravidade de Doença
Transdução de Sinais
Células Th1/efeitos dos fármacos
Células Th1/imunologia
Células Th1/virologia
Células Th17/efeitos dos fármacos
Células Th17/imunologia
Células Th17/virologia
Fator A de Crescimento do Endotélio Vascular/antagonistas & inibidores
Fator A de Crescimento do Endotélio Vascular/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Antiviral Agents); 0 (Ccl2 protein, mouse); 0 (Chemokine CCL2); 0 (Chemokine CXCL2); 0 (Cxcl2 protein, mouse); 0 (Interleukins); 0 (MicroRNAs); 0 (Vascular Endothelial Growth Factor A); 0 (resolvin D1); 0 (vascular endothelial growth factor A, mouse); 25167-62-8 (Docosahexaenoic Acids); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 3.4.24.35 (Mmp9 protein, mouse); R16CO5Y76E (Aspirin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170607
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.3HI1216-511RR


  9 / 1609 MEDLINE  
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[PMID]:28522730
[Au] Autor:Mylonas KJ; Turner NA; Bageghni SA; Kenyon CJ; White CI; McGregor K; Kimmitt RA; Sulston R; Kelly V; Walker BR; Porter KE; Chapman KE; Gray GA
[Ad] Endereço:University/BHF Centre for Cardiovascular ScienceUniversity of Edinburgh, Queen's Medical Research Institute, Edinburgh, UK.
[Ti] Título:11ß-HSD1 suppresses cardiac fibroblast CXCL2, CXCL5 and neutrophil recruitment to the heart post MI.
[So] Source:J Endocrinol;233(3):315-327, 2017 Jun.
[Is] ISSN:1479-6805
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We have previously demonstrated that neutrophil recruitment to the heart following myocardial infarction (MI) is enhanced in mice lacking 11ß-hydroxysteroid dehydrogenase type 1 (11ß-HSD1) that regenerates active glucocorticoid within cells from intrinsically inert metabolites. The present study aimed to identify the mechanism of regulation. In a mouse model of MI, neutrophil mobilization to blood and recruitment to the heart were higher in 11ß-HSD1-deficient ( ) relative to wild-type (WT) mice, despite similar initial injury and circulating glucocorticoid. In bone marrow chimeric mice, neutrophil mobilization was increased when 11ß-HSD1 was absent from host cells, but not when absent from donor bone marrow-derived cells. Consistent with a role for 11ß-HSD1 in 'host' myocardium, gene expression of a subset of neutrophil chemoattractants, including the chemokines and , was selectively increased in the myocardium of mice relative to WT. SM22α-Cre directed disruption of in smooth muscle and cardiomyocytes had no effect on neutrophil recruitment. Expression of and was elevated in fibroblast fractions isolated from hearts of mice post MI and provision of either corticosterone or of the 11ß-HSD1 substrate, 11-dehydrocorticosterone, to cultured murine cardiac fibroblasts suppressed IL-1α-induced expression of and These data identify suppression of CXCL2 and CXCL5 chemoattractant expression by 11ß-HSD1 as a novel mechanism with potential for regulation of neutrophil recruitment to the injured myocardium, and cardiac fibroblasts as a key site for intracellular glucocorticoid regeneration during acute inflammation following myocardial injury.
[Mh] Termos MeSH primário: 11-beta-Hidroxiesteroide Desidrogenase Tipo 1/metabolismo
Quimiocina CXCL2/metabolismo
Quimiocina CXCL5/metabolismo
Fibroblastos/fisiologia
Neutrófilos/fisiologia
[Mh] Termos MeSH secundário: 11-beta-Hidroxiesteroide Desidrogenase Tipo 1/genética
Animais
Células da Medula Óssea
Células Cultivadas
Quimiocina CXCL5/genética
Corticosterona/análogos & derivados
Corticosterona/farmacologia
Masculino
Camundongos
Camundongos Knockout
Proteínas dos Microfilamentos/genética
Proteínas dos Microfilamentos/metabolismo
Proteínas Musculares/genética
Proteínas Musculares/metabolismo
Infarto do Miocárdio
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL2); 0 (Chemokine CXCL5); 0 (Microfilament Proteins); 0 (Muscle Proteins); 0 (transgelin); EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenase Type 1); FO4V44A3G3 (11-dehydrocorticosterone); W980KJ009P (Corticosterone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170520
[St] Status:MEDLINE
[do] DOI:10.1530/JOE-16-0501


  10 / 1609 MEDLINE  
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[PMID]:28415997
[Au] Autor:Mei X; Wang HX; Li JS; Liu XH; Lu XF; Li Y; Zhang WY; Tian YG
[Ad] Endereço:Basic Medicine College, Henan University of Chinese Medicine, Zhengzhou, Henan, 450046, China.
[Ti] Título:Dusuqing granules (DSQ) suppress inflammation in Klebsiella pneumonia rat via NF-κB/MAPK signaling.
[So] Source:BMC Complement Altern Med;17(1):216, 2017 Apr 17.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Dusuqing granules (DSQ) have been used in the treatment of bacterial pneumonia clinically, with remarkable benefits. This study was initiated to explore the effects of DSQ on pulmonary inflammation by regulating nuclear factor (NF)-κB/mitogen-activated protein kinase (MAPK) signaling in bacterial pneumonia rats. METHODS: Rat model was duplicated with Klebsiella pneumonia by a one-time intratracheal injection. Rats were randomized into control, model, DSQ and levofloxacin (LVX) groups. After administrated with appropriate medicines for 7 days, lung tissues were harvested and prepared for pathological analysis, and interleukin (IL)-1, IL-6, monocyte chemotactic protein (MCP)-1and macrophage inflammatory protein (MIP)-2 detections. NF-κB mRNA was measured by real-time qPCR, and the phosphorylation and total proteins of P38MAPK, JNK46/54, ERK42/44 were determined by Western blotting. RESULTS: Marked pathological impairments were observed in model rats, whereas were improved in DSQ group. The cytokines levels, NF-κB mRNA expression and the phosphorylation of P38MAPK, JNK46/54 and ERK42/44 proteins were significantly higher in model group, and were significantly depressed in DSQ group. CONCLUSION: The protective effects of DSQ on Klebsiella pneumonia might be attributed to its inactivative effects of NF-κB/ MAPK pathway.
[Mh] Termos MeSH primário: Medicamentos de Ervas Chinesas/farmacologia
Infecções por Klebsiella/metabolismo
Klebsiella pneumoniae
Proteínas Quinases Ativadas por Mitógeno/metabolismo
NF-kappa B/metabolismo
Pneumonia Bacteriana/metabolismo
Pneumonia/metabolismo
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/farmacologia
Anti-Inflamatórios/uso terapêutico
Quimiocina CCL2/metabolismo
Quimiocina CXCL2/metabolismo
Medicamentos de Ervas Chinesas/uso terapêutico
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Feminino
Interleucinas/metabolismo
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Infecções por Klebsiella/tratamento farmacológico
Infecções por Klebsiella/microbiologia
Infecções por Klebsiella/patologia
Pulmão/efeitos dos fármacos
Pulmão/metabolismo
Magnoliopsida
Masculino
Fosforilação
Fitoterapia
Pneumonia/tratamento farmacológico
Pneumonia/microbiologia
Pneumonia Bacteriana/tratamento farmacológico
Pneumonia Bacteriana/microbiologia
Pneumonia Bacteriana/patologia
Ratos Sprague-Dawley
Transdução de Sinais
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Chemokine CCL2); 0 (Chemokine CXCL2); 0 (Cxcl2 protein, rat); 0 (Drugs, Chinese Herbal); 0 (Interleukins); 0 (NF-kappa B); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170419
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-1736-x



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