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  1 / 11116 MEDLINE  
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[PMID]:29304171
[Au] Autor:Galán A; Mayer I; Rafaj RB; Bendelja K; Susic V; Cerón JJ; Mrljak V
[Ad] Endereço:ERA Chair project ''VetMedZg'', Clinic for Internal Diseases, Faculty of Veterinary Medicine, University of Zagreb, Zagreb, Croatia.
[Ti] Título:MCP-1, KC-like and IL-8 as critical mediators of pathogenesis caused by Babesia canis.
[So] Source:PLoS One;13(1):e0190474, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Canine babesiosis caused by the intraerythrocytic protozoan parasite Babesia canis is a tick-borne disease characterized by a host response that involves both cellular and humoral immunity. This study focuses on the secretion of cytokines Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF), Keratinocyte Chemotactic-like (KC-like), Interleukins (IL)-2, IL-7, IL-8, IL-10, IL-15, IL-18 and Monocyte Chemotactic Protein-1 (MCP-1) in babesiosis caused by Babesia canis upon treatment with Imizol®. We assessed time dependent changes in cytokine levels and tested whether these changes correlate with pathogenesis of the disease. Sixteen healthy dogs and 31 dogs infected with Babesia canis, of which 18 showed complications, were treated with Imizol®. One dog died during the study (3.2%). Longitudinal study was perfomed by monitoring dogs at the first day of presentation (day 1) and 6 days later (day 7). Our results show that higher MCP-1 levels on day 1 are positively associated with the occurrence of complications, (complicated vs. uncomplicated; p = 0.00016). A similar pattern was observed for KC-like on day 1 (p = 0.0326) and day 7 (p = 0.044). Moreover, babesiosis caused by B. canis produced a steady increase in IL-8 levels with a moderate to strong negative correlation with erythrocyte counts and hematocrit in uncomplicated diseased dogs only (Spearman's rank correlation coefficient rs = -0.582 and rs = -0.598 respectively). Like for MCP-1, KC-like levels also differed in complicated and uncomplicated diseased dogs on day 1 (p = 0.03236) and day 7 (p = 0.044). Furthermore, KC-like levels were strongly correlated with IL-8 levels (rs = 0.663-0.7) and non-segmented neutrophil counts (rs = 0.572-0.732) in both diseased groups. Analysis of ROC suggests the use of serum levels of MCP-1 and IL-7 as predictors of the occurrence of complications with an AUC of 0.906 and 0.896 respectively and linear combinations of MCP-1, KC-Like, IL-7 and GM-CSF with values up to AUC = 0.983. Cytokine cluster analysis presented in this study can contribute to a better understanding of the pathogenesis of babesiosis and serve as a prognostic tool for the early detection of cases with highest likelihood of developing complications. Overall, our studies show that infection by B. canis elicits a cytokine pattern that is distinct from that observed with B. rossi, and that some of the inflammatory mediators can be useful to predict complications. Our results also suggest targets for the development of novel therapeutic strategies in babesiosis caused by B. canis.
[Mh] Termos MeSH primário: Babesia/patogenicidade
Babesiose/fisiopatologia
Quimiocina CCL2/secreção
Quimiocinas/fisiologia
Doenças do Cão/fisiopatologia
Fator Estimulador de Colônias de Granulócitos e Macrófagos/secreção
Interleucina-8/secreção
[Mh] Termos MeSH secundário: Animais
Babesiose/parasitologia
Quimiocina CCL2/fisiologia
Doenças do Cão/parasitologia
Cães
Fator Estimulador de Colônias de Granulócitos e Macrófagos/fisiologia
Interleucina-8/fisiologia
Estudos Longitudinais
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chemokine CCL2); 0 (Chemokines); 0 (Interleukin-8); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190474


  2 / 11116 MEDLINE  
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[PMID]:29390552
[Au] Autor:Sang GY; Meng CR; Hao YF; Dai JH
[Ad] Endereço:Laboratory Medicine Diagnostic Centre.
[Ti] Título:Monocyte chemoattractant protein-1 (MCP-1)-2518 A/G polymorphism and lupus nephritis risk: A PRISMA-compliant meta-analysis.
[So] Source:Medicine (Baltimore);96(51):e9401, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Monocyte chemoattractant protein-1 (MCP-1) plays an important role in the development of allergic inflammatory reactions by recruiting various immune cells, which is associated with many autoimmune diseases, but the association with the MCP-1-2518A/G gene polymorphism and lupus nephritis (LN) was still controversial in previous studies. Thus, we performed a meta-analysis to derive a more precise evaluation of the association between MCP-1 -2518A/G polymorphism and LN risk and evaluated influence of ethnicity and source of controls. METHODS: A systematic review and meta-analysis that will be performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). Relevant literatures dated to September 2016 were acquired from the PubMed, EMBASE, Cochran Library databases. A total of 961 LN cases and 1867 controls were extracted from 10 published case-control studies. We used odds ratios (OR) with 95% confidence intervals (CI) to assess the risk of LN with MCP-1-2518A/G. RESULTS: Our meta-analysis suggested that MCP-1-2518A/G polymorphism was associated with the risk of LN (GG vs AG+AA: P < .01, OR = 1.42, 95% CI: 1.13-1.79 and A vs G P = .02, OR = 0.74, 95% CI: 0.58-0.95). Then the subgroup analysis showed MCP-1 -2518 A/G gene has a certain correlation with LN susceptibility in the American population (GG vs AA: P < .01, OR = 5.70, 95% CI: 2.09-15.50, GG vs AG+AA: P < .01, OR = 3.31, 95% CI: 1.97-5.54, GG+AG vs AA: P < .01, OR = 2.86, 95% CI: 1.14-7.18, and A vs G: P < .01, OR = 0.43, 95% CI: 0.24-0.79), while no significant risk in Europeans and Asians. CONCLUSION: The current meta-analysis suggests that the MCP-1-2518A/G polymorphism is associated with an increased risk of LN, especially in the American population. However, better-designed studies with larger sample sizes are needed to validate the results.
[Mh] Termos MeSH primário: Quimiocina CCL2/genética
Predisposição Genética para Doença
Nefrite Lúpica/genética
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Marcadores Genéticos
Seres Humanos
Nefrite Lúpica/etnologia
Modelos Estatísticos
Razão de Chances
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (CCL2 protein, human); 0 (Chemokine CCL2); 0 (Genetic Markers)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009401


  3 / 11116 MEDLINE  
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[PMID]:28458349
[Au] Autor:Matsutani T; Tamura K; Kutsukake M; Matsuda A; Tachikawa E; Uchida E
[Ad] Endereço:Department of Gastrointestinal and Hepato-Biliary-Pancreatic Surgery, Nippon Medical School.
[Ti] Título:Impact of Pioglitazone on Macrophage Dynamics in Adipose Tissues of Cecal Ligation and Puncture-Treated Mice.
[So] Source:Biol Pharm Bull;40(5):638-644, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Pioglitazone improves sepsis-induced organ injury accompanied with anti-inflammatory effects on visceral adipose tissue. However, its action in adipose immune cells remains to be ascertained. We investigated the effects of pioglitazone on visceral adipose macrophage population and polarisation in cecal ligation and puncture (CLP)-induced sepsis mice. Eight-week-old male mice were assigned to 3 groups: 1) sham-operated group, 2) CLP group, or 3) pioglitazone-treated CLP group. Pioglitazone (10 mg/kg) was injected intraperitonally for 7 d and CLP surgery was performed. Visceral adipose tissues were collected 24 h after the surgery. mRNA expression of several macrophage markers (inducible nitric oxide synthase (iNOS) for M1, arginase1 (Arg1) and interleukin (IL)-10 for M2, CD163 and F4/80 for mature macrophages) and inflammatory adipokines (IL-6, monocyte chemoattractant protein-1: MCP-1) was quantified by real-time RT-PCR. Tissue sections were subjected to the immunohistochemical analysis and the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) assay. CLP significantly enhanced Arg1, IL-10 and iNOS mRNA expressions as compared with the sham group, and pioglitazone significantly increased the mRNA level of CD163 and F4/80 in CLP mice. Expression of IL-6 and MCP-1 stimulated by CLP was reduced by pioglitazone treatment. Increased CD11b/c- and CD163-positive cells as well as apoptotic cells were observed in the CLP group and the pioglitazone-treated group. The data indicate that M1/M2 macrophage activation of visceral adipose tissues is induced in CLP-induced mice, and the function of macrophages recruited from surrounding organs may be modulated by pioglitazone treatment.
[Mh] Termos MeSH primário: Hipoglicemiantes/farmacologia
Gordura Intra-Abdominal/patologia
Macrófagos/efeitos dos fármacos
Sepse/patologia
Tiazolidinedionas/farmacologia
[Mh] Termos MeSH secundário: Adipocinas/metabolismo
Animais
Arginase/análise
Biomarcadores/análise
Ceco
Quimiocina CCL2/metabolismo
Hipoglicemiantes/administração & dosagem
Injeções Intraperitoneais
Interleucina-10/sangue
Ligadura
Masculino
Camundongos
Punções
Tiazolidinedionas/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adipokines); 0 (Biomarkers); 0 (Ccl2 protein, mouse); 0 (Chemokine CCL2); 0 (Hypoglycemic Agents); 0 (IL10 protein, mouse); 0 (Thiazolidinediones); 130068-27-8 (Interleukin-10); EC 3.5.3.1 (Arg1 protein, mouse); EC 3.5.3.1 (Arginase); X4OV71U42S (pioglitazone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-00883


  4 / 11116 MEDLINE  
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[PMID]:29176318
[Au] Autor:Tang Y; Jia W; Niu X; Wu L; Shen H; Wang L; Qi R; Ling C; Li M
[Ad] Endereço:Military Hygiene Department, Faculty of Naval Medicine, Second Military Medical University, Shanghai, China.
[Ti] Título:CCL2 is Upregulated by Decreased miR-122 Expression in Iron-Overload-Induced Hepatic Inflammation.
[So] Source:Cell Physiol Biochem;44(3):870-883, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Iron overload (IO) is accompanied by hepatic inflammation. The chemokine (C-C motif) ligand 2 (CCL2) mediates inflammation, and its overexpression is associated with IO. However, whether IO results in CCL2 overexpression in the liver and the underlying mechanisms are unclear. METHODS: We subjected mice to IO by administering intraperitoneal injections of dextran-iron or by feeding mice a 3% dextran-iron diet to observe the effects of IO on miR-122/CCL2 expression through real-time qPCR and Western blot analysis. We also used indicators, including the expression of the inflammatory cytokine, the inflammation score based on H&E staining and the serum content of ALT and AST to evaluate the effects of IO on hepatic inflammation. Meanwhile, we observed the effects of vitamin E on IO-induced hepatic inflammation. In cells, we used 100 µΜ FeSO4 or 30 µΜ Holo-Tf to produce IO and observed the roles of miR-122 in regulating CCL2 expression by using miR-122 mimics or inhibitors to overexpress or inhibit miR-122. Then, we used a dual-luciferase reporter assay to prove that miR-122 regulates CCL2 expression through direct binding to its complementary sequence in the CCL2 mRNA 3'UTR. RESULTS: IO induces the downregulation of miR-122 and the upregulation of CCL2, as well as inflammatory responses both in vitro and in vivo. Although IO-induced oxidative stress is eliminated by the antioxidant vitamin E, IO-induced hepatic inflammation still exists, which probably can be explained by the fact that vitamin E has no effects on the miR-122/CCL2 pathway. In in vitro experiments, the overexpression and inhibition of miR-122 significantly reduced and increased CCL2 expression, respectively. The dual-luciferase reporter assay indicates that miR-122 binds CCL2 mRNA 3'UTR. CONCLUSION: We propose the roles of miR-122/CCL2 in IO-induced hepatic inflammation. Our studies should provide a new clue for developing clinical strategies for patients with IO.
[Mh] Termos MeSH primário: Quimiocina CCL2/metabolismo
Complexo Ferro-Dextran/toxicidade
Fígado/patologia
MicroRNAs/metabolismo
Regulação para Cima/efeitos dos fármacos
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Antagomirs/metabolismo
Sequência de Bases
Linhagem Celular
Quimiocina CCL2/antagonistas & inibidores
Quimiocina CCL2/genética
Compostos Ferrosos/toxicidade
Seres Humanos
Inflamação
Interleucina-6/sangue
Ferro/análise
Ferro/sangue
Fígado/efeitos dos fármacos
Fígado/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
MicroRNAs/antagonistas & inibidores
MicroRNAs/genética
Estresse Oxidativo/efeitos dos fármacos
Alinhamento de Sequência
Fator de Transcrição RelA/genética
Fator de Transcrição RelA/metabolismo
Transferrina/farmacologia
Fator de Necrose Tumoral alfa/sangue
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
Vitamina E/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Antagomirs); 0 (Chemokine CCL2); 0 (Ferrous Compounds); 0 (Interleukin-6); 0 (MicroRNAs); 0 (Mirn122 microRNA, mouse); 0 (Transcription Factor RelA); 0 (Transferrin); 0 (Tumor Necrosis Factor-alpha); 1406-18-4 (Vitamin E); 39R4TAN1VT (ferrous sulfate); 9004-66-4 (Iron-Dextran Complex); E1UOL152H7 (Iron)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485355


  5 / 11116 MEDLINE  
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[PMID]:28466296
[Au] Autor:Suryawanashi YR; Zhang T; Woyczesczyk HM; Christie J; Byers E; Kohler S; Eversole R; Mackenzie C; Essani K
[Ad] Endereço:Laboratory of Virology, Department of Biological Sciences, Western Michigan University, Kalamazoo, MI, 49008-5410, USA.
[Ti] Título:T-independent response mediated by oncolytic tanapoxvirus recombinants expressing interleukin-2 and monocyte chemoattractant protein-1 suppresses human triple negative breast tumors.
[So] Source:Med Oncol;34(6):112, 2017 Jun.
[Is] ISSN:1559-131X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human triple negative breast cancer (TNBC) is an aggressive disease, associated with a high rate of recurrence and metastasis. Current therapeutics for TNBC are limited, highly toxic and show inconsistent efficacy due to a high degree of intra-tumoral and inter-tumoral heterogeneity. Oncolytic viruses (OVs) are an emerging treatment option for cancers. Several OVs are currently under investigation in preclinical and clinical settings. Here, we examine the oncolytic potential of two tanapoxvirus (TPV) recombinants expressing mouse monocyte chemoattractant protein (mMCP)-1 [also known as mCCL2] and mouse interleukin (mIL)-2, in human TNBC, in vitro and in vivo. Both wild-type (wt) TPV and TPV recombinants demonstrated efficient replicability in human TNBC cells and killed cancer cell efficiently in a dose-dependent manner in vitro. TPV/∆66R/mCCL2 and TPV/∆66R/mIL-2 expressing mCCL2 and mIL-2, respectively, suppressed the growth of MDA-MB-231 tumor xenografts in nude mice significantly, as compared to the mock-injected tumors. Histological analysis of tumors showed areas of viable tumor cells, necrotic foci and immune cell accumulation in virus-treated tumors. Moreover, TPV/∆66R/mIL-2-treated tumors showed a deep infiltration of mononuclear immune cells into the tumor capsule and focal cell death in tumors. In conclusion, TPV recombinants expressing mCCL2 and mIL-2 showed a significant therapeutic effect in MDA-MB-231 tumor xenografts, in nude mice through induction of potent antitumor immune responses. Considering the oncolytic potency of armed oncolytic TPV recombinants expressing mCCL2 and mIL-2 in an experimental nude mouse model, these viruses merit further investigation as alternative treatment options for human breast cancer.
[Mh] Termos MeSH primário: Quimiocina CCL2/metabolismo
Imunoterapia/métodos
Interleucina-2/metabolismo
Vírus Oncolíticos/genética
Neoplasias de Mama Triplo Negativas/metabolismo
Yatapoxvirus/genética
[Mh] Termos MeSH secundário: Animais
Aotidae
Linhagem Celular
Quimiocina CCL2/genética
Quimiocina CCL2/imunologia
Seres Humanos
Interleucina-2/genética
Interleucina-2/imunologia
Masculino
Camundongos
Camundongos Nus
Vírus Oncolíticos/metabolismo
Neoplasias de Mama Triplo Negativas/genética
Neoplasias de Mama Triplo Negativas/imunologia
Ensaios Antitumorais Modelo de Xenoenxerto
Yatapoxvirus/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CCL2); 0 (Interleukin-2)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180111
[Lr] Data última revisão:
180111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1007/s12032-017-0973-7


  6 / 11116 MEDLINE  
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[PMID]:29236764
[Au] Autor:Kim BY; Son Y; Lee J; Choi J; Kim CD; Bae SS; Eo SK; Kim K
[Ad] Endereço:Department of Pharmacology, Pusan National University-School of Medicine, Yangsan, Gyeongnam, Republic of Korea.
[Ti] Título:Dexamethasone inhibits activation of monocytes/macrophages in a milieu rich in 27-oxygenated cholesterol.
[So] Source:PLoS One;12(12):e0189643, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Molecular mechanisms underlying the decreased number of macrophages and T cells in the arteries of cholesterol-fed-rabbits following dexamethasone administration are unknown. We investigated the possibility that dexamethasone could affect activation of monocytic cells induced by oxygenated derivatives of cholesterol (oxysterols) using THP-1 monocyte/macrophage cells. 27-Hydroxycholesterol (27OHChol), an oxysterol elevated with hypercholesterolemia, enhanced production of CCL2, known as MCP1, chemokine from monocytes/macrophages and migration of the monocytic cells, but the CCL2 production and the cell migration were reduced by treatment with dexamethasone. Dexamethasone inhibited superproduction of CCL2 induced by 27OHChol plus LPS and attenuated transcription of matrix metalloproteinase 9 as well as secretion of its active gene product induced by 27OHChol. The drug downregulated cellular and surface levels of CD14 and blocked release of soluble CD14 without altering transcription of the gene. Dexamethasone also inhibited expression and phosphorylation of the NF-κB p65 subunit enhanced by 27OHChol. Collectively, these results indicate that dexamethasone inhibits activation of monocytes/macrophages in response to 27OHChol, thereby leading to decreased migration of inflammatory cells in milieu rich in oxygenated derivatives of cholesterol.
[Mh] Termos MeSH primário: Dexametasona/farmacologia
Hidroxicolesteróis/metabolismo
Macrófagos/efeitos dos fármacos
Monócitos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Linhagem Celular
Quimiocina CCL2/biossíntese
Quimiocina CCL2/metabolismo
Quimiotaxia de Leucócito
Regulação para Baixo
Seres Humanos
Macrófagos/imunologia
Macrófagos/metabolismo
Monócitos/imunologia
Monócitos/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fator de Transcrição RelA/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL2 protein, human); 0 (Chemokine CCL2); 0 (Hydroxycholesterols); 0 (Transcription Factor RelA); 6T2NA6P5SQ (27-hydroxycholesterol); 7S5I7G3JQL (Dexamethasone)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189643


  7 / 11116 MEDLINE  
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[PMID]:29176798
[Au] Autor:Woodcock TM; Frugier T; Nguyen TT; Semple BD; Bye N; Massara M; Savino B; Besio R; Sobacchi C; Locati M; Morganti-Kossmann MC
[Ad] Endereço:National Trauma Research Institute, The Alfred Hospital, Melbourne, Australia.
[Ti] Título:The scavenging chemokine receptor ACKR2 has a significant impact on acute mortality rate and early lesion development after traumatic brain injury.
[So] Source:PLoS One;12(11):e0188305, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The atypical chemokine receptor ACKR2 promotes resolution of acute inflammation by operating as a scavenger receptor for inflammatory CC chemokines in several experimental models of inflammatory disorders, however its role in the brain remains unclear. Based on our previous reports of increased expression of inflammatory chemokines and their corresponding receptors following traumatic brain injury (TBI), we hypothesised that ACKR2 modulates neuroinflammation following brain trauma and that its deletion exacerbates cellular inflammation and chemokine production. We demonstrate increased CCL2 and ACKR2 mRNA expression in post-mortem human brain, whereby ACKR2 mRNA levels correlated with later times post-TBI. This data is consistent with the transient upregulation of ACKR2 observed in mouse brain after closed head injury (CHI). As compared to WT animals, ACKR2-/- mice showed a higher mortality rate after CHI, while the neurological outcome in surviving mice was similar. At day 1 post-injury, ACKR2-/- mice displayed aggravated lesion volume and no differences in CCL2 expression and macrophage recruitment relative to WT mice. Reciprocal regulation of ACKR2 and CCL2 expression was explored in cultured astrocytes, which are recognized as the major source of CCL2 and also express ACKR2. ACKR2 mRNA increased as early as 2 hours after an inflammatory challenge in WT astrocytes. As expected, CCL2 expression also dramatically increased at 4 hours in WT astrocytes but was significantly lower in ACKR2-/- astrocytes, possibly indicating a co-regulation of CCL2 and ACKR2 in these cells. Conversely, in vivo, CCL2 mRNA/protein levels were increased similarly in ACKR2-/- and WT brains at 4 and 12 hours after CHI, in line with the lack of differences in cerebral macrophage recruitment and neurological recovery. In conclusion, ACKR2 is induced after TBI and has a significant impact on mortality and lesion development acutely following CHI, while its role in chemokine expression, macrophage activation, brain pathology, and neurological recovery at later time-points is minor. Concordant to evidence in multiple sclerosis experimental models, our data corroborate a distinct role for ACKR2 in cerebral inflammatory processes compared to its reported functions in peripheral tissues.
[Mh] Termos MeSH primário: Lesões Encefálicas Traumáticas/metabolismo
Lesões Encefálicas Traumáticas/mortalidade
Receptores de Quimiocinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Astrócitos/metabolismo
Astrócitos/patologia
Osso e Ossos/patologia
Encéfalo/metabolismo
Encéfalo/patologia
Encéfalo/fisiopatologia
Lesões Encefálicas Traumáticas/genética
Lesões Encefálicas Traumáticas/fisiopatologia
Células Cultivadas
Quimiocina CCL2/genética
Quimiocina CCL2/metabolismo
Deleção de Genes
Seres Humanos
Inflamação/patologia
Macrófagos/metabolismo
Macrófagos/patologia
Masculino
Camundongos Endogâmicos C57BL
Mortalidade
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptores de Quimiocinas/genética
Recuperação de Função Fisiológica
Regulação para Cima/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCBP2 protein, human); 0 (Ccbp2 protein, mouse); 0 (Chemokine CCL2); 0 (RNA, Messenger); 0 (Receptors, Chemokine)
[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:171128
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188305


  8 / 11116 MEDLINE  
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[PMID]:29182510
[Au] Autor:Soe HJ; Khan AM; Manikam R; Samudi Raju C; Vanhoutte P; Sekaran SD
[Ad] Endereço:1​Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
[Ti] Título:High dengue virus load differentially modulates human microvascular endothelial barrier function during early infection.
[So] Source:J Gen Virol;98(12):2993-3007, 2017 Dec.
[Is] ISSN:1465-2099
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Plasma leakage is the main pathophysiological feature in severe dengue, resulting from altered vascular barrier function associated with an inappropriate immune response triggered upon infection. The present study investigated functional changes using an electric cell-substrate impedance sensing system in four (brain, dermal, pulmonary and retinal) human microvascular endothelial cell (MEC) lines infected with purified dengue virus, followed by assessment of cytokine profiles and the expression of inter-endothelial junctional proteins. Modelling of changes in electrical impedance suggests that vascular leakage in dengue-infected MECs is mostly due to the modulation of cell-to-cell interactions, while this loss of vascular barrier function observed in the infected MECs varied between cell lines and DENV serotypes. High levels of inflammatory cytokines (IL-6 and TNF-α), chemokines (CXCL1, CXCL5, CXCL11, CX3CL1, CCL2 and CCL20) and adhesion molecules (VCAM-1) were differentially produced in the four infected MECs. Further, the tight junctional protein, ZO-1, was down-regulated in both the DENV-1-infected brain and pulmonary MECs, while claudin-1, PECAM-1 and VE-cadherin were differentially expressed in these two MECs after infection. Non-purified virus stock was also studied to investigate the impact of virus stock purity on dengue-specific immune responses, and the results suggest that virus stock propagated through cell culture may include factors that mask or alter the DENV-specific immune responses of the MECs. The findings of the present study show that high DENV load differentially modulates human microvascular endothelial barrier function and disrupts the function of inter-endothelial junctional proteins during early infection with organ-specific cytokine production.
[Mh] Termos MeSH primário: Células Endoteliais/virologia
Endotélio Vascular/virologia
Interações Hospedeiro-Patógeno
Carga Viral/imunologia
[Mh] Termos MeSH secundário: Antígenos CD/genética
Antígenos CD/imunologia
Encéfalo/citologia
Encéfalo/imunologia
Encéfalo/virologia
Caderinas/genética
Caderinas/imunologia
Linhagem Celular
Quimiocina CCL2/genética
Quimiocina CCL2/imunologia
Quimiocina CCL20/genética
Quimiocina CCL20/imunologia
Quimiocina CX3CL1/genética
Quimiocina CX3CL1/imunologia
Quimiocinas CXC/genética
Quimiocinas CXC/imunologia
Claudina-1/genética
Claudina-1/imunologia
Vírus da Dengue/genética
Vírus da Dengue/crescimento & desenvolvimento
Vírus da Dengue/imunologia
Derme/citologia
Derme/imunologia
Derme/virologia
Impedância Elétrica
Células Endoteliais/citologia
Células Endoteliais/imunologia
Endotélio Vascular/citologia
Endotélio Vascular/imunologia
Regulação da Expressão Gênica
Seres Humanos
Interleucina-6/genética
Interleucina-6/imunologia
Pulmão/citologia
Pulmão/imunologia
Pulmão/virologia
Especificidade de Órgãos
Permeabilidade
Molécula-1 de Adesão Celular Endotelial de Plaquetas/genética
Molécula-1 de Adesão Celular Endotelial de Plaquetas/imunologia
Retina/citologia
Retina/imunologia
Retina/virologia
Transdução de Sinais
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
Molécula 1 de Adesão de Célula Vascular/genética
Molécula 1 de Adesão de Célula Vascular/imunologia
Internalização do Vírus
Proteína da Zônula de Oclusão-1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (CCL2 protein, human); 0 (CCL20 protein, human); 0 (CX3CL1 protein, human); 0 (Cadherins); 0 (Chemokine CCL2); 0 (Chemokine CCL20); 0 (Chemokine CX3CL1); 0 (Chemokines, CXC); 0 (Claudin-1); 0 (IL6 protein, human); 0 (Interleukin-6); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (TJP1 protein, human); 0 (Tumor Necrosis Factor-alpha); 0 (Vascular Cell Adhesion Molecule-1); 0 (Zonula Occludens-1 Protein); 0 (cadherin 5)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171213
[Lr] Data última revisão:
171213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1099/jgv.0.000981


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[PMID]:29183044
[Au] Autor:Blokhuis C; Doeleman S; Cohen S; Demirkaya N; Scherpbier HJ; Kootstra NA; Kuhle J; Teunissen CE; Verbraak FD; Pajkrt D
[Ad] Endereço:Department of Hematology, Immunology and Infectious Diseases, Emma Children's Hospital/Academic Medical Center, University of Amsterdam, The Netherlands.
[Ti] Título:Inflammatory and Neuronal Biomarkers Associated With Retinal Thinning in Pediatric HIV.
[So] Source:Invest Ophthalmol Vis Sci;58(13):5985-5992, 2017 Nov 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: The pathophysiology of neuroretinal thinning in children with human immunodeficiency virus (HIV) is poorly understood. The current study aimed to assess whether neuroretinal thinning in clinically stable perinatally HIV-infected children was associated with biomarkers of immune activation, inflammation, and neuronal damage. Methods: Inflammation-associated and neuronal damage markers were measured in blood and cerebrospinal fluid (CSF) of HIV-infected children aged 8 to 18 years. Using mixed-effects regression analyses, we assessed associations between these biomarkers and neuroretinal layer thickness, as measured with spectral-domain optical coherence tomography. Results: Thirty-two HIV-infected children (median age 13.6 years, 50% male) were included. Blood plasma levels of interleukin-6, monocyte chemoattractant protein-1, and soluble intercellular adhesion molecule-1 were inversely correlated with foveal inner plexiform layer thickness (coef = -4.40, P < 0.001; coef = -9.67, P = 0.047; coef = -10.48, P = 0.042, respectively). Plasma interleukin-6 was inversely correlated with foveal ganglion cell layer thickness (coef = -2.49, P = 0.010). Total Tau levels in CSF were inversely correlated with outer nuclear layer and inner segments thickness (foveal: coef = -19.3, P = 0.029; pericentral: coef = -18.09, P = 0.006) and pericentral total retinal thickness (coef = -28.2, P = 0.017). Conclusions: Neuroretinal thinning was associated with inflammation-associated and neuronal injury biomarkers in a cohort of antiretroviral therapy-treated perinatally HIV-infected children. These findings suggest that ongoing immune activation, inflammation, and neuronal injury occur in parallel with retinal thinning in pediatric HIV.
[Mh] Termos MeSH primário: Infecções por HIV/complicações
Retina/patologia
Degeneração Retiniana
[Mh] Termos MeSH secundário: Adolescente
Biomarcadores/sangue
Biomarcadores/líquido cefalorraquidiano
Quimiocina CCL2/sangue
Criança
Feminino
Seres Humanos
Molécula 1 de Adesão Intercelular/sangue
Interleucinas/sangue
Masculino
Análise de Regressão
Degeneração Retiniana/sangue
Degeneração Retiniana/líquido cefalorraquidiano
Degeneração Retiniana/patologia
Células Ganglionares da Retina/patologia
Tomografia de Coerência Óptica
Proteínas tau/líquido cefalorraquidiano
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Chemokine CCL2); 0 (Interleukins); 0 (tau Proteins); 126547-89-5 (Intercellular Adhesion Molecule-1)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171201
[Lr] Data última revisão:
171201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-22252


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[PMID]:28745689
[Au] Autor:Bulanov NM; Serova AG; Kuznetsova EI; Bulanova ML; Novikov PI; Kozlovskaya LV; Moiseev SV
[Ad] Endereço:I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia, Moscow, Russia.
[Ti] Título:[Kidney injury molecules (KIM-1, MCP-1) and type IV collagen in the assessment of activity of antineutrophil cytoplasmic antibody-associated glomerulonephritis].
[Ti] Título:Molekuly povrezhdeniia pochechnoi tkani (KIM-1, MCP-1) i kollagen IV tipa v otsenke aktivnosti assotsiirovannogo s antineitrofil'nymi tsitoplazmaticheskimi antitelami glomerulonefrita..
[So] Source:Ter Arkh;89(6):48-55, 2017.
[Is] ISSN:0040-3660
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:AIM: To assess the significance of determining the serum and urinary concentrations of monocyte chemotactic protein-1 (MCP-1), kidney injury molecule-1 (KIM-1), and type IV collagen in patients with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) to estimate the activity of renal involvement in AAV. SUBJECTS AND METHODS: 78 patients (32 men and 46 women) (median age 55 (45; 61) years) with AAV were examined. The patients were divided into 3 groups according to the AAV activity estimated using the Birmingham vasculitis activity Score (BVAS): 1) 25 patients with active ANCA-associated glomerulonephritis (GN); 2) 26 patients with active AAV without renal involvement; 3) 27 patients in sustained AAV remission. The serum and urinary concentrations of the markers were measured by enzyme immunoassay. RESULTS: The urinary concentration of all 3 biomarkers was higher in patients with renal involvement (Group 1); the differences in the levels of MCP-1 and type IV collagen were statistically significant as compared to Groups 2 and 3 (p<0.01), while that in KIM-1 level was only in Group 2. There were statistically significant correlations between the urinary concentration of these biomarkers and the traditional GN activity indices (erythrocyturia, daily proteinuria (DPU), total BVAS scores that reflect renal involvement, as well as serum creatinine levels and estimated glomerular filtration rate (p<0.05). ROC curve analysis showed that the urinary MCP-1 excretion of ≥159 pg/ml had the highest (92%) sensitivity and urinary type IV collagen excretion of ≥3.09 µg/l had the highest (86%) specificity in assessing the activity of ANCA-associated GN. At the same time, their diagnostic value increased in terms of a combination of DPU and ESR (96% sensitivity, 84.9% specificity). CONCLUSION: The urinary excretion of MCP-1, KIM-1, and type IV collagen reflects the severity of local renal inflammation in AAV patients and a study of these indicators is a promising diagnostic tool for assessing the activity of ANCA-associated GN.
[Mh] Termos MeSH primário: Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos
Anticorpos Anticitoplasma de Neutrófilos/imunologia
Quimiocina CCL2
Colágeno Tipo IV
Glomerulonefrite
Receptor Celular 1 do Vírus da Hepatite A
[Mh] Termos MeSH secundário: Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/sangue
Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/imunologia
Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/urina
Biomarcadores/sangue
Biomarcadores/urina
Quimiocina CCL2/sangue
Quimiocina CCL2/imunologia
Quimiocina CCL2/urina
Colágeno Tipo IV/sangue
Colágeno Tipo IV/imunologia
Colágeno Tipo IV/urina
Feminino
Glomerulonefrite/sangue
Glomerulonefrite/imunologia
Glomerulonefrite/urina
Receptor Celular 1 do Vírus da Hepatite A/sangue
Receptor Celular 1 do Vírus da Hepatite A/imunologia
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Antineutrophil Cytoplasmic); 0 (Biomarkers); 0 (CCL2 protein, human); 0 (Chemokine CCL2); 0 (Collagen Type IV); 0 (HAVCR1 protein, human); 0 (Hepatitis A Virus Cellular Receptor 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171129
[Lr] Data última revisão:
171129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.17116/terarkh201789648-55



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