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  1 / 2045 MEDLINE  
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[PMID]:28954264
[Au] Autor:Pan Q; Feng Y; Peng Y; Zhou H; Deng Z; Li L; Han H; Lin J; Shi L; Wang S; An N; Yang C; Liu HF
[Ti] Título:Basophil Recruitment to Skin Lesions of Patients with Systemic Lupus Erythematosus Mediated by CCR1 and CCR2.
[So] Source:Cell Physiol Biochem;43(2):832-839, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Basophils have been reported to infiltrate skin lesions in various skin diseases, but not in systemic lupus erythematosus (SLE). This study investigated basophil infiltration in SLE and its mechanism. METHODS: Twenty newly diagnosed SLE patients and twenty healthy controls were enrolled. Nine SLE patients underwent skin biopsies. Flow cytometric analysis the phenotype of peripheral basophils and their migration rate toward RANTES and MCP-1 were analyzed with the transwell culture system, also the expression of these two chemokines in skin tissue were analyzed with immunohistochemistry. RESULTS: Increased activation and decreased numbers of peripheral basophils were observed in SLE patients compared with controls. Basophil migration into skin lesions of SLE patients were observed, but not in normal skin tissue. This migration was related to the upregulation of chemokine receptors CCR1 and CCR2 on basophils. In vitro studies showed that migration rate toward RANTES and MCP-1 increased significantly in basophils from SLE patients compared with those from controls. Consistently, high levels of RANTES and MCP-1 expression were observed in skin lesions from SLE patients but not in normal skin tissue. CONCLUSION: Basophil recruitment to skin lesions of SLE patients mediated by CCR1 and CCR2, which may contribute to tissue damage in SLE.
[Mh] Termos MeSH primário: Basófilos/patologia
Lúpus Eritematoso Sistêmico/patologia
Receptores CCR1/imunologia
Receptores CCR2/imunologia
Pele/patologia
[Mh] Termos MeSH secundário: Adulto
Basófilos/imunologia
Movimento Celular
Quimiocina CCL2/análise
Quimiocina CCL2/imunologia
Quimiocina CCL5/análise
Quimiocina CCL5/imunologia
Feminino
Seres Humanos
Lúpus Eritematoso Sistêmico/imunologia
Masculino
Receptores CCR1/análise
Receptores CCR2/análise
Pele/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL2 protein, human); 0 (CCR1 protein, human); 0 (CCR2 protein, human); 0 (Chemokine CCL2); 0 (Chemokine CCL5); 0 (Receptors, CCR1); 0 (Receptors, CCR2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE
[do] DOI:10.1159/000481609


  2 / 2045 MEDLINE  
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[PMID]:28892735
[Au] Autor:Kholodnyuk I; Rudevica Z; Leonciks A; Ehlin-Henriksson B; Kashuba E
[Ad] Endereço:A. Kirchenstein Institute of Microbiology and Virology, Riga Stradins University (RSU), 5 Ratsupites str, 1067 Riga, Latvia; Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, 16 Nobels väg, Box 280, 171 77 Stockholm, Sweden. Electronic address: irina.holodnuka@rsu.lv.
[Ti] Título:Expression of the chemokine receptors CCR1 and CCR2B is up-regulated in peripheral blood B cells upon EBV infection and in established lymphoblastoid cell lines.
[So] Source:Virology;512:1-7, 2017 Dec.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In immunocompetent individuals, EBV establishes in B cells an asymptomatic lifelong latent infection controlled by the immune system. Chemokine receptors regulate immune system function. CCR1 and CCR2 share protein sequence similarity and exert responses to multiple chemokines. The role of these receptors in B cells is largely unknown. We show that the mRNA and functional protein expression of CCR1 and CCR2 is induced in ex vivo B cells upon EBV infection and in established lymphoblastoid cell lines (LCLs). The CCR1 and CCR2B ORF transcripts were determined in LCLs. In contrast, in both the EBV-negative and EBV-positive Burkitt lymphoma cell lines, neither the CCR1, CCR2A, and CCR2B ORF transcripts nor their corresponding proteins were detected. Our data suggest that CCR1/CCR2B could be involved in clearing EBV-infected latency III B cells in immunocompetent individuals via directing the migration of these cells and attracting the chemokines-expressing immune cells.
[Mh] Termos MeSH primário: Linfócitos B/metabolismo
Regulação da Expressão Gênica/fisiologia
Herpesvirus Humano 4/fisiologia
Receptores CCR1/metabolismo
Receptores CCR2/metabolismo
Regulação para Cima
[Mh] Termos MeSH secundário: Linfócitos B/virologia
Linhagem Celular
Seres Humanos
Proteínas Nucleares/genética
Proteínas Nucleares/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptores CCR1/genética
Receptores CCR2/genética
Ativação Transcricional
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCR1 protein, human); 0 (Nuclear Proteins); 0 (RNA, Messenger); 0 (Receptors, CCR1); 0 (Receptors, CCR2); 0 (SND1 protein, human)
[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:170912
[St] Status:MEDLINE


  3 / 2045 MEDLINE  
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[PMID]:28851810
[Au] Autor:DeBerge M; Yeap XY; Dehn S; Zhang S; Grigoryeva L; Misener S; Procissi D; Zhou X; Lee DC; Muller WA; Luo X; Rothlin C; Tabas I; Thorp EB
[Ad] Endereço:From the Department of Pathology and Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, IL (M.D., X.Y.Y., S.D., S.Z., L.G., S.M., D.P., X.Z., D.C.Le., W.A.M., X.L., E.B.T.); Division of Molecular Medicine at Columbia University, New York (I.T.)
[Ti] Título:MerTK Cleavage on Resident Cardiac Macrophages Compromises Repair After Myocardial Ischemia Reperfusion Injury.
[So] Source:Circ Res;121(8):930-940, 2017 Sep 29.
[Is] ISSN:1524-4571
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Clinical benefits of reperfusion after myocardial infarction are offset by maladaptive innate immune cell function, and therapeutic interventions are lacking. OBJECTIVE: We sought to test the significance of phagocytic clearance by resident and recruited phagocytes after myocardial ischemia reperfusion. METHODS AND RESULTS: In humans, we discovered that clinical reperfusion after myocardial infarction led to significant elevation of the soluble form of MerTK (myeloid-epithelial-reproductive tyrosine kinase; ie, soluble MER), a critical biomarker of compromised phagocytosis by innate macrophages. In reperfused mice, macrophage deficiency led to decreased cardiac wound debridement, increased infarct size, and depressed cardiac function, newly implicating MerTK in cardiac repair after myocardial ischemia reperfusion. More notably, ) mice, which are resistant to cleavage, showed significantly reduced infarct sizes and improved systolic function. In contrast to other cardiac phagocyte subsets, resident cardiac MHCII CCR2 (major histocompatibility complex II/C-C motif chemokine receptor type 2) macrophages expressed higher levels of MerTK and, when exposed to apoptotic cells, secreted proreparative cytokines, including transforming growth factor-ß. deficiency compromised the accumulation of MHCII phagocytes, and this was rescued in ) mice. Interestingly, blockade of CCR2-dependent monocyte infiltration into the heart reduced soluble MER levels post-ischemia reperfusion. CONCLUSIONS: Our data implicate monocyte-induced MerTK cleavage on proreparative MHCII cardiac macrophages as a novel contributor and therapeutic target of reperfusion injury.
[Mh] Termos MeSH primário: Macrófagos/enzimologia
Traumatismo por Reperfusão Miocárdica/enzimologia
Miocárdio/enzimologia
Proteínas Proto-Oncogênicas/metabolismo
Receptores Proteína Tirosina Quinases/metabolismo
Infarto do Miocárdio com Supradesnível do Segmento ST/enzimologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Citocinas/imunologia
Citocinas/metabolismo
Modelos Animais de Doenças
Feminino
Predisposição Genética para Doença
Antígenos de Histocompatibilidade Classe II/imunologia
Antígenos de Histocompatibilidade Classe II/metabolismo
Seres Humanos
Imunidade Inata
Macrófagos/imunologia
Macrófagos/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Meia-Idade
Monócitos/enzimologia
Monócitos/imunologia
Traumatismo por Reperfusão Miocárdica/imunologia
Traumatismo por Reperfusão Miocárdica/patologia
Traumatismo por Reperfusão Miocárdica/fisiopatologia
Miocárdio/imunologia
Miocárdio/patologia
Fagocitose
Fenótipo
Proteólise
Proteínas Proto-Oncogênicas/deficiência
Proteínas Proto-Oncogênicas/genética
Proteínas Proto-Oncogênicas/imunologia
Receptores Proteína Tirosina Quinases/deficiência
Receptores Proteína Tirosina Quinases/genética
Receptores Proteína Tirosina Quinases/imunologia
Receptores CCR2/genética
Receptores CCR2/imunologia
Receptores CCR2/metabolismo
Infarto do Miocárdio com Supradesnível do Segmento ST/imunologia
Infarto do Miocárdio com Supradesnível do Segmento ST/patologia
Infarto do Miocárdio com Supradesnível do Segmento ST/fisiopatologia
Transdução de Sinais
Fatores de Tempo
c-Mer Tirosina Quinase
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccr2 protein, mouse); 0 (Cytokines); 0 (Histocompatibility Antigens Class II); 0 (Proto-Oncogene Proteins); 0 (Receptors, CCR2); EC 2.7.10.1 (MERTK protein, human); EC 2.7.10.1 (Mertk protein, mouse); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); EC 2.7.10.1 (c-Mer Tyrosine Kinase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170831
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCRESAHA.117.311327


  4 / 2045 MEDLINE  
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[PMID]:28836736
[Au] Autor:Cédile O; Wlodarczyk A; Owens T
[Ad] Endereço:Department of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark.
[Ti] Título:CCL2 recruits T cells into the brain in a CCR2-independent manner.
[So] Source:APMIS;125(11):945-956, 2017 Nov.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:CCL2 is a chemokine that can be induced during neuroinflammation to recruit immune cells, but its role in the central nervous system (CNS) is unclear. Our aim was to better understand its role. We induced CCL2 in CNS of naive CCL2-deficient mice using intrathecally administered replication-defective adenovirus and examined cell infiltration by flow cytometry. CCL2 expression induced pronounced and unexpected recruitment of regulatory and IFNγ-producing T cells to CNS from blood, possibly related to defective egress of monocytes from CCL2-deficient bone marrow. Infiltration also occurred in mice lacking CCR2, a receptor for CCL2. Expression of another receptor for CCL2, CCR4, and CXCR3, a receptor for CXCL10, which was also induced, were both increased in CCL2-treated CNS. CCR4 was expressed by neurons and astrocytes as well as CD4 T cells, and CXCR3 was expressed by CD4 and CD8 T cells. Chemokine-recruited T cells did not lead to CNS pathology. Our findings show a role for CCL2 in recruitment of CD4 T cells to the CNS and show that redundancy among chemokine receptors ensures optimal response.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Sistema Nervoso Central/imunologia
Quimiocina CCL2/imunologia
Receptores CCR2/imunologia
[Mh] Termos MeSH secundário: Adenoviridae/genética
Adenoviridae/metabolismo
Animais
Astrócitos/citologia
Astrócitos/imunologia
Linfócitos T CD4-Positivos/citologia
Linfócitos T CD8-Positivos/citologia
Movimento Celular
Sistema Nervoso Central/citologia
Quimiocina CCL2/deficiência
Quimiocina CCL2/genética
Quimiocina CXCL10/genética
Quimiocina CXCL10/imunologia
Feminino
Regulação da Expressão Gênica
Genes Reporter
Vetores Genéticos/química
Vetores Genéticos/metabolismo
Injeções Espinhais
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Camundongos
Camundongos Knockout
Neurônios/citologia
Neurônios/imunologia
Receptores CCR2/genética
Receptores CCR4/genética
Receptores CCR4/imunologia
Receptores CXCR3/genética
Receptores CXCR3/imunologia
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/imunologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccl2 protein, mouse); 0 (Ccr2 protein, mouse); 0 (Ccr4 protein, mouse); 0 (Chemokine CCL2); 0 (Chemokine CXCL10); 0 (Cxcl10 protein, mouse); 0 (Cxcr3 protein, mouse); 0 (Luminescent Proteins); 0 (Receptors, CCR2); 0 (Receptors, CCR4); 0 (Receptors, CXCR3); 0 (Recombinant Fusion Proteins); 0 (red fluorescent protein)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170825
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12740


  5 / 2045 MEDLINE  
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[PMID]:28799208
[Au] Autor:Lebrun A; Lo Re S; Chantry M; Izquierdo Carerra X; Uwambayinema F; Ricci D; Devosse R; Ibouraadaten S; Brombin L; Palmai-Pallag M; Yakoub Y; Pasparakis M; Lison D; Huaux F
[Ad] Endereço:Louvain Centre for Toxicology and Applied Pharmacology (LTAP), Institut de Recherche Experimentale et Clinique (IREC), Université catholique de Louvain, Brussels, Belgium.
[Ti] Título:CCR2 monocytic myeloid-derived suppressor cells (M-MDSCs) inhibit collagen degradation and promote lung fibrosis by producing transforming growth factor-ß1.
[So] Source:J Pathol;243(3):320-330, 2017 Nov.
[Is] ISSN:1096-9896
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Monocytes infiltrating scar tissue are predominantly viewed as progenitor cells. Here, we show that tissue CCR2 monocytes have specific immunosuppressive and profibrotic functions. CCR2 monocytic cells are acutely recruited to the lung before the onset of silica-induced fibrosis in mice. These tissue monocytes are defined as monocytic myeloid-derived suppressor cells (M-MDSCs) because they significantly suppress T-lymphocyte proliferation in vitro. M-MDSCs collected from silica-treated mice also express transforming growth factor (TGF)-ß1, which stimulates lung fibroblasts to release tissue inhibitor of metalloproteinase (TIMP)-1, an inhibitor of metalloproteinase collagenolytic activity. By using LysMCreCCR2 mice, we show that limiting CCR2 M-MDSC accumulation reduces the pulmonary contents of TGF-ß1, TIMP-1 and collagen after silica treatment. M-MDSCs do not differentiate into lung macrophages, granulocytes or fibrocytes during pulmonary fibrogenesis. Collectively, our data indicate that M-MDSCs contribute to lung fibrosis by specifically promoting a non-degrading collagen microenvironment. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
[Mh] Termos MeSH primário: Monócitos/metabolismo
Células Supressoras Mieloides/citologia
Fibrose Pulmonar/metabolismo
Receptores CCR2/metabolismo
Fator de Crescimento Transformador beta1/metabolismo
[Mh] Termos MeSH secundário: Animais
Proliferação Celular/fisiologia
Colágeno/metabolismo
Pulmão/patologia
Ativação Linfocitária/fisiologia
Camundongos Endogâmicos C57BL
Fibrose Pulmonar/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, CCR2); 0 (Transforming Growth Factor beta1); 9007-34-5 (Collagen)
[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:170812
[St] Status:MEDLINE
[do] DOI:10.1002/path.4956


  6 / 2045 MEDLINE  
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[PMID]:28716963
[Au] Autor:Tian DS; Peng J; Murugan M; Feng LJ; Liu JL; Eyo UB; Zhou LJ; Mogilevsky R; Wang W; Wu LJ
[Ad] Endereço:Department of Neurology, Tongji Hospital, and.
[Ti] Título:Chemokine CCL2-CCR2 Signaling Induces Neuronal Cell Death via STAT3 Activation and IL-1ß Production after Status Epilepticus.
[So] Source:J Neurosci;37(33):7878-7892, 2017 Aug 16.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Elevated levels of chemokine C-C motif ligand 2 (CCL2) and its receptor CCR2 have been reported in patients with temporal lobe epilepsy and in experimental seizures. However, the functional significance and molecular mechanism underlying CCL2-CCR2 signaling in epileptic brain remains largely unknown. In this study, we found that the upregulated CCL2 was mainly expressed in hippocampal neurons and activated microglia from mice 1 d after kainic acid (KA)-induced seizures. Taking advantage of double-transgenic mice, we demonstrated that CCL2-CCR2 signaling has a role in resident microglial activation and blood-derived monocyte infiltration. Moreover, seizure-induced degeneration of neurons in the hippocampal CA3 region was attenuated in mice lacking CCL2 or CCR2. We further showed that CCR2 activation induced STAT3 (signal transducer and activator of transcription 3) phosphorylation and IL-1ß production, which are critical for promoting neuronal cell death after status epilepticus. Consistently, pharmacological inhibition of STAT3 by WP1066 reduced seizure-induced IL-1ß production and subsequent neuronal death. Two weeks after KA-induced seizures, CCR2 deficiency not only reduced neuronal loss, but also attenuated seizure-induced behavioral impairments, including anxiety, memory decline, and recurrent seizure severity. Together, we demonstrated that CCL2-CCR2 signaling contributes to neurodegeneration via STAT3 activation and IL-1ß production after status epilepticus, providing potential therapeutic targets for the treatment of epilepsy. Epilepsy is a global concern and epileptic seizures occur in many neurological conditions. Neuroinflammation associated with microglial activation and monocyte infiltration are characteristic of epileptic brains. However, molecular mechanisms underlying neuroinflammation in neuronal death following epilepsy remain to be elucidated. Here we demonstrate that CCL2-CCR2 signaling is required for monocyte infiltration, which in turn contributes to kainic acid (KA)-induced neuronal cell death. The downstream of CCR2 activation involves STAT3 (signal transducer and activator of transcription 3) phosphorylation and IL-1ß production. Two weeks after KA-induced seizures, CCR2 deficiency not only reduced neuronal loss, but also attenuated seizure-induced behavioral impairments, including anxiety, memory decline, and recurrent seizure severity. The current study provides a novel insight on the function and mechanisms of CCL2-CCR2 signaling in KA-induced neurodegeneration and behavioral deficits.
[Mh] Termos MeSH primário: Quimiocina CCL2/metabolismo
Interleucina-1beta/biossíntese
Neurônios/metabolismo
Receptores CCR2/metabolismo
Fator de Transcrição STAT3/metabolismo
Estado Epiléptico/metabolismo
[Mh] Termos MeSH secundário: Animais
Morte Celular/fisiologia
Feminino
Hipocampo/metabolismo
Hipocampo/patologia
Masculino
Camundongos
Camundongos Knockout
Neurônios/patologia
Receptores CCR2/deficiência
Estado Epiléptico/patologia
Estado Epiléptico/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccl2 protein, mouse); 0 (Ccr2 protein, mouse); 0 (Chemokine CCL2); 0 (Interleukin-1beta); 0 (Receptors, CCR2); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse)
[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:170719
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0315-17.2017


  7 / 2045 MEDLINE  
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[PMID]:28715799
[Au] Autor:He Y; Xu X; Zhu T; Tang M; Mei J; Si Y
[Ad] Endereço:Department of Cardiovascular Surgery, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
[Ti] Título:Resident Arterial Cells and Circulating Bone Marrow-Derived Cells both Contribute to Intimal Hyperplasia in a Rat Allograft Carotid Transplantation Model.
[So] Source:Cell Physiol Biochem;42(4):1303-1312, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Neointimal formation following vascular injury remains a major mechanism of restenosis, whereas the precise sources of neointimal cells are still uncertain. We tested the hypothesis that both injured arterial cells and non-arterial cells contribute to intimal hyperplasia. METHODS: Following allograft transplantation of the balloon-injured carotid common artery (n = 3-6), the cellular composition of the transplant grafts and the origins of neointimal cells were measured by immunohistochemistry and immunofluorescence staining. RESULTS: Smooth muscle actin (SMA)-positive and CD68-positive cells were clearly observed 14 days later in the neointima after allograft transplantation of the balloon-injured carotid common artery, where re-endothelialization was not yet complete. Green fluorescent protein (GFP) and wild-type (WT) allograft transplantation revealed that the majority of the neointima cells were apparently from the recipient (≈85%) versus the donor (≈15%). Both monocyte chemotactic protein-1 (MCP-1)/CCR2 and stromal cell-derived factor-1 (SDF-1)/CXCR4 signaling were involved in intimal hyperplasia, with bone marrow-derived cells also playing a role. CONCLUSION: These data support the hypothesis that intimal hyperplasia could develop in our novel rat allograft transplantation model of arterial injury, where neointima is attributable not only to local arterial cells but also non-arterial cells including the bone marrow.
[Mh] Termos MeSH primário: Células da Medula Óssea/patologia
Lesões das Artérias Carótidas/patologia
Artéria Carótida Primitiva/patologia
Células Endoteliais/patologia
Neointima/patologia
Transplante de Tecidos
Túnica Íntima/lesões
[Mh] Termos MeSH secundário: Actinas/genética
Actinas/imunologia
Animais
Antígenos CD/genética
Antígenos CD/imunologia
Antígenos de Diferenciação Mielomonocítica/genética
Antígenos de Diferenciação Mielomonocítica/imunologia
Células da Medula Óssea/imunologia
Lesões das Artérias Carótidas/genética
Lesões das Artérias Carótidas/imunologia
Lesões das Artérias Carótidas/cirurgia
Artéria Carótida Primitiva/imunologia
Artéria Carótida Primitiva/cirurgia
Linhagem da Célula/imunologia
Rastreamento de Células
Quimiocina CCL2/genética
Quimiocina CCL2/imunologia
Quimiocina CXCL12/genética
Quimiocina CXCL12/imunologia
Células Endoteliais/imunologia
Regulação da Expressão Gênica
Genes Reporter
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/imunologia
Neointima/genética
Neointima/imunologia
Neointima/cirurgia
Ratos
Ratos Endogâmicos Lew
Ratos Transgênicos
Receptores CCR2/genética
Receptores CCR2/imunologia
Receptores CXCR4/genética
Receptores CXCR4/imunologia
Transdução de Sinais
Transplante Homólogo
Túnica Íntima/imunologia
Túnica Íntima/cirurgia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CD68 protein, rat); 0 (CXCL12 protein, rat); 0 (Ccl2 protein, rat); 0 (Ccr2 protein, rat); 0 (Chemokine CCL2); 0 (Chemokine CXCL12); 0 (Cxcr4 protein, rat); 0 (Receptors, CCR2); 0 (Receptors, CXCR4); 0 (smooth muscle actin, rat); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE
[do] DOI:10.1159/000478959


  8 / 2045 MEDLINE  
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[PMID]:28710250
[Au] Autor:Morse K; Kimizuka Y; Chan MPK; Shibata M; Shimaoka Y; Takeuchi S; Forbes B; Nirschl C; Li B; Zeng Y; Bronson RT; Katagiri W; Shigeta A; Sîrbulescu RF; Chen H; Tan RYY; Tsukada K; Brauns T; Gelfand J; Sluder A; Locascio JJ; Poznansky MC; Anandasabapathy N; Kashiwagi S
[Ad] Endereço:Vaccine and Immunotherapy Center, Division of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Charlestown, MA 02129.
[Ti] Título:Near-Infrared 1064 nm Laser Modulates Migratory Dendritic Cells To Augment the Immune Response to Intradermal Influenza Vaccine.
[So] Source:J Immunol;199(4):1319-1332, 2017 Aug 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Brief exposure of skin to near-infrared (NIR) laser light has been shown to augment the immune response to intradermal vaccination and thus act as an immunologic adjuvant. Although evidence indicates that the NIR laser adjuvant has the capacity to activate innate subsets including dendritic cells (DCs) in skin as conventional adjuvants do, the precise immunological mechanism by which the NIR laser adjuvant acts is largely unknown. In this study we sought to identify the cellular target of the NIR laser adjuvant by using an established mouse model of intradermal influenza vaccination and examining the alteration of responses resulting from genetic ablation of specific DC populations. We found that a continuous wave (CW) NIR laser adjuvant broadly modulates migratory DC (migDC) populations, specifically increasing and activating the Lang and CD11b Lang subsets in skin, and that the Ab responses augmented by the CW NIR laser are dependent on DC subsets expressing CCR2 and Langerin. In comparison, a pulsed wave NIR laser adjuvant showed limited effects on the migDC subsets. Our vaccination study demonstrated that the efficacy of the CW NIR laser is significantly better than that of the pulsed wave laser, indicating that the CW NIR laser offers a desirable immunostimulatory microenvironment for migDCs. These results demonstrate the unique ability of the NIR laser adjuvant to selectively target specific migDC populations in skin depending on its parameters, and highlight the importance of optimization of laser parameters for desirable immune protection induced by an NIR laser-adjuvanted vaccine.
[Mh] Termos MeSH primário: Células Dendríticas/imunologia
Vacinas contra Influenza/imunologia
Raios Infravermelhos
Lasers
Pele/imunologia
Pele/efeitos da radiação
Vacinação/métodos
[Mh] Termos MeSH secundário: Adjuvantes Imunológicos
Animais
Antígenos de Superfície/metabolismo
Movimento Celular
Células Dendríticas/fisiologia
Vacinas contra Influenza/administração & dosagem
Injeções Intradérmicas
Lectinas Tipo C/metabolismo
Lectinas de Ligação a Manose/metabolismo
Camundongos
Receptores CCR2/genética
Receptores CCR2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Antigens, Surface); 0 (Ccr2 protein, mouse); 0 (Cd207 protein, mouse); 0 (Influenza Vaccines); 0 (Lectins, C-Type); 0 (Mannose-Binding Lectins); 0 (Receptors, CCR2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170716
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601873


  9 / 2045 MEDLINE  
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[PMID]:28696252
[Au] Autor:Williams JW; Elvington A; Ivanov S; Kessler S; Luehmann H; Baba O; Saunders BT; Kim KW; Johnson MW; Craft CS; Choi JH; Sorci-Thomas MG; Zinselmeyer BH; Brestoff JR; Liu Y; Randolph GJ
[Ad] Endereço:From the Department of Pathology and Immunology (J.W.W., A.E., S.I., S.K., O.B., B.T.S., K.-W.K., M.W.J., J.-H.C., B.H.Z., J.R.B., G.J.R.), Department of Radiology (H.L., Y.L.), and Department of Medicine, Division of Bone and Mineral Diseases (C.S.C.), Washington University School of Medicine, St.
[Ti] Título:Thermoneutrality but Not UCP1 Deficiency Suppresses Monocyte Mobilization Into Blood.
[So] Source:Circ Res;121(6):662-676, 2017 Sep 01.
[Is] ISSN:1524-4571
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Ambient temperature is a risk factor for cardiovascular disease. Cold weather increases cardiovascular events, but paradoxically, cold exposure is metabolically protective because of UCP1 (uncoupling protein 1)-dependent thermogenesis. OBJECTIVE: We sought to determine the differential effects of ambient environmental temperature challenge and UCP1 activation in relation to cardiovascular disease progression. METHODS AND RESULTS: Using mouse models of atherosclerosis housed at 3 different ambient temperatures, we observed that cold temperature enhanced, whereas thermoneutral housing temperature inhibited atherosclerotic plaque growth, as did deficiency in UCP1. However, whereas UCP1 deficiency promoted poor glucose tolerance, thermoneutral housing enhanced glucose tolerance, and this effect held even in the context of UCP1 deficiency. In conditions of thermoneutrality, but not UCP1 deficiency, circulating monocyte counts were reduced, likely accounting for fewer monocytes entering plaques. Reductions in circulating blood monocytes were also found in a large human cohort in correlation with environmental temperature. By contrast, reduced plaque growth in mice lacking UCP1 was linked to lower cholesterol. Through application of a positron emission tomographic tracer to track CCR2 cell localization and intravital 2-photon imaging of bone marrow, we associated thermoneutrality with an increased monocyte retention in bone marrow. Pharmacological activation of ß3-adrenergic receptors applied to mice housed at thermoneutrality induced UCP1 in beige fat pads but failed to promote monocyte egress from the marrow. CONCLUSIONS: Warm ambient temperature is, like UCP1 deficiency, atheroprotective, but the mechanisms of action differ. Thermoneutrality associates with reduced monocyte egress from the bone marrow in a UCP1-dependent manner in mice and likewise may also suppress blood monocyte counts in man.
[Mh] Termos MeSH primário: Aterosclerose/metabolismo
Monócitos/fisiologia
Termogênese
Proteína Desacopladora 1/genética
[Mh] Termos MeSH secundário: Animais
Aterosclerose/sangue
Aterosclerose/patologia
Aterosclerose/fisiopatologia
Movimento Celular
Colesterol/metabolismo
Temperatura Baixa
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Monócitos/metabolismo
Placa Aterosclerótica/sangue
Placa Aterosclerótica/metabolismo
Receptores CCR2/genética
Receptores CCR2/metabolismo
Proteína Desacopladora 1/deficiência
Proteína Desacopladora 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccr2 protein, mouse); 0 (Receptors, CCR2); 0 (Ucp1 protein, mouse); 0 (Uncoupling Protein 1); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCRESAHA.117.311519


  10 / 2045 MEDLINE  
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[PMID]:28692738
[Au] Autor:Chong RS; Lee YS; Chu SWL; Toh LZ; Wong TTL
[Ad] Endereço:Singapore National Eye Centre, Singapore 2Singapore Eye Research Institute, Singapore 3Duke NUS Graduate Medical School, Singapore.
[Ti] Título:Inhibition of Monocyte Chemoattractant Protein 1 Prevents Conjunctival Fibrosis in an Experimental Model of Glaucoma Filtration Surgery.
[So] Source:Invest Ophthalmol Vis Sci;58(9):3432-3439, 2017 Jul 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: To evaluate the effect of treatment with monocyte chemoattractant protein-1 receptor inhibitor (MCP-Ri) to maintain bleb survival and prevent fibrosis in an experimental model of glaucoma filtration surgery (GFS). Methods: GFS was performed on one eye of C57/Bl6 mice (n = 36) that was treated with MCP-Ri, mitomycin-C (MMC), or vehicle at the time of surgery. Real-time polymerase chain reaction was used to evaluate conjunctival expression of monocyte chemoattractant protein-1 (MCP-1), TGFB1, TGFB2, collagen 1a1 (Col1a1), sparc (Sparc), and fibronectin at 2 and 7 days following surgery. Anterior segment slit-lamp examination, optical coherence tomography, and confocal microscopy were performed in vivo at day 14. Eyes were processed for immunohistochemical staining of F4/80, a monocyte-macrophage marker, at day 2. In vitro experiments were also performed to compare the effect of MMC, MCP-Ri, and vehicle on the viability of mouse Tenon's fibroblasts. Results: Treatment with MCP-Ri results in a greater reduction in the percentage of F4/80-positive cells in conjunctival blebs and lesser MCP-1 gene expression following experimental GFS than MMC or control. Both MMC and MCP-Ri reduced Col1a1 and Sparc expression, but not fibronectin. TGFB1 decreased with MCP-Ri but not MMC; MMC but not MCP-Ri reduced TGFB2. MMC and MCP-Ri treatment resulted in the preservation of bleb height at day 14, as compared to control. MCP-Ri was less toxic to mouse Tenon's fibroblasts in comparison with MMC. Conclusions: Targeting MCP-1 results in prolonged bleb survival following experimental GFS with less cellular toxicity as compared to MMC. MCP inhibition could provide a safer alternative to conventional antifibrotic adjunctive treatments in GFS.
[Mh] Termos MeSH primário: Antifibrinolíticos/farmacologia
Quimiocina CCL2/antagonistas & inibidores
Túnica Conjuntiva/efeitos dos fármacos
Inibidores Enzimáticos/farmacologia
Fibroblastos/efeitos dos fármacos
Fibrose/prevenção & controle
Implantes para Drenagem de Glaucoma
Glaucoma/tratamento farmacológico
Receptores CCR2/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Sobrevivência Celular/efeitos dos fármacos
Quimiocina CCL2/metabolismo
Colágeno/metabolismo
Modelos Animais de Doenças
Fibronectinas/metabolismo
Cirurgia Filtrante
Glaucoma/cirurgia
Camundongos
Camundongos Endogâmicos C57BL
Mitomicina/farmacocinética
Osteonectina/metabolismo
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antifibrinolytic Agents); 0 (Chemokine CCL2); 0 (Enzyme Inhibitors); 0 (Fibronectins); 0 (Osteonectin); 0 (Receptors, CCR2); 0 (SPARC protein, mouse); 0 (Transforming Growth Factor beta); 50SG953SK6 (Mitomycin); 9007-34-5 (Collagen)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170711
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-21480



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