Base de dados : MEDLINE
Pesquisa : A11.627 [Categoria DeCS]
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[PMID]:29191879
[Au] Autor:Engblom C; Pfirschke C; Zilionis R; Da Silva Martins J; Bos SA; Courties G; Rickelt S; Severe N; Baryawno N; Faget J; Savova V; Zemmour D; Kline J; Siwicki M; Garris C; Pucci F; Liao HW; Lin YJ; Newton A; Yaghi OK; Iwamoto Y; Tricot B; Wojtkiewicz GR; Nahrendorf M; Cortez-Retamozo V; Meylan E; Hynes RO; Demay M; Klein A; Bredella MA; Scadden DT; Weissleder R; Pittet MJ
[Ad] Endereço:Center for Systems Biology, Massachusetts General Hospital Research Institute and Harvard Medical School, Boston, MA 02114, USA.
[Ti] Título:Osteoblasts remotely supply lung tumors with cancer-promoting SiglecF neutrophils.
[So] Source:Science;358(6367), 2017 12 01.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone marrow-derived myeloid cells can accumulate within tumors and foster cancer outgrowth. Local immune-neoplastic interactions have been intensively investigated, but the contribution of the systemic host environment to tumor growth remains poorly understood. Here, we show in mice and cancer patients ( = 70) that lung adenocarcinomas increase bone stromal activity in the absence of bone metastasis. Animal studies reveal that the cancer-induced bone phenotype involves bone-resident osteocalcin-expressing (Ocn ) osteoblastic cells. These cells promote cancer by remotely supplying a distinct subset of tumor-infiltrating SiglecF neutrophils, which exhibit cancer-promoting properties. Experimentally reducing Ocn cell numbers suppresses the neutrophil response and lung tumor outgrowth. These observations posit osteoblasts as remote regulators of lung cancer and identify SiglecF neutrophils as myeloid cell effectors of the osteoblast-driven protumoral response.
[Mh] Termos MeSH primário: Adenocarcinoma/patologia
Antígenos CD/metabolismo
Antígenos de Diferenciação Mielomonocítica/metabolismo
Osso e Ossos/patologia
Lectinas/metabolismo
Neoplasias Pulmonares/patologia
Infiltração de Neutrófilos
Neutrófilos/metabolismo
Neutrófilos/patologia
Osteoblastos/patologia
[Mh] Termos MeSH secundário: Animais
Densidade Óssea
Células da Medula Óssea/patologia
Osso e Ossos/metabolismo
Linhagem Celular Tumoral
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Células Mieloides/patologia
Neoplasias Experimentais/patologia
Osteocalcina/metabolismo
Receptor para Produtos Finais de Glicação Avançada/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (Lectins); 0 (Receptor for Advanced Glycation End Products); 0 (SIGLEC5 protein, human); 0 (sRAGE protein, human); 104982-03-8 (Osteocalcin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE


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[PMID]:28747346
[Au] Autor:Nagalingam G; Vinuesa CG; Britton WJ; Saunders BM
[Ad] Endereço:Tuberculosis Research Program, Centenary Institute, Newtown, New South Wales 2042, Australia.
[Ti] Título:Modulation of Roquin Function in Myeloid Cells Reduces -Induced Inflammation.
[So] Source:J Immunol;199(5):1796-1804, 2017 09 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Damaging inflammation is a hallmark of infection, and understanding how this is regulated is important for the development of new therapies to limit excessive inflammation. The E3 ubiquitin ligase, Roquin, is involved in immune regulation; however, its role in immunity to is unknown. To address this, we infected mice with a point mutation in ( ). Aerosol-infected mice showed enhanced control of infection associated with delayed bacterial dissemination and upregulated TNF production in the lungs after 2 wk. However, this early control of infection was not maintained, and by 8 wk postinfection mice demonstrated an increased bacterial burden and dysregulated inflammation in the lungs. As the inflammation in the lungs of the mice could have been influenced by emerging autoimmune conditions that are characteristic of the mice aging, the function of Roquin was examined in immune cell subsets in the absence of autoimmune complications. bacillus Calmette-Guérin-primed T cells transferred into mice provided equivalent protection in the spleen and liver. Interestingly, the transfer of mycobacteria-specific (P25 CD4 TCR transgenic) wild-type spleen cells into mice actually led to enhanced protection with reduced bacterial load, decreased chemokine expression, and reduced inflammation in the lungs compared with transfers into mice expressing intact Roquin. These studies suggest that modulation of Roquin in myeloid cells may reduce both inflammation and bacterial growth during the chronic phase of infection.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Inflamação/imunologia
Pulmão/imunologia
Mycobacterium tuberculosis/fisiologia
Células Mieloides/imunologia
Tuberculose/imunologia
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Animais
Carga Bacteriana
Linfócitos T CD4-Positivos/microbiologia
Linfócitos T CD4-Positivos/transplante
Células Cultivadas
Pulmão/microbiologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Células Mieloides/microbiologia
Quimeras de Transplante
Fator de Necrose Tumoral alfa/metabolismo
Ubiquitina-Proteína Ligases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Tumor Necrosis Factor-alpha); EC 2.3.2.27 (Rc3h1 protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1602069


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[PMID]:28463086
[Au] Autor:Mann EH; Ho TR; Pfeffer PE; Matthews NC; Chevretton E; Mudway I; Kelly FJ; Hawrylowicz CM
[Ad] Endereço:1 MRC and Asthma-UK Centre for Allergic Mechanisms in Asthma, and.
[Ti] Título:Vitamin D Counteracts an IL-23-Dependent IL-17A IFN-γ Response Driven by Urban Particulate Matter.
[So] Source:Am J Respir Cell Mol Biol;57(3):355-366, 2017 09.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Urban particulate matter (UPM) air pollution and vitamin D deficiency are detrimentally associated with respiratory health. This is hypothesized to be due in part to regulation of IL-17A, which UPM is reported to promote. Here, we used a myeloid dendritic cell (DC)-memory CD4 T cell co-culture system to characterize UPM-driven IL-17A cells, investigate the mechanism by which UPM-primed DCs promote this phenotype, and address evidence for cross-regulation by vitamin D. CD1c myeloid DCs were cultured overnight with or without a reference source of UPM and/or active vitamin D (1,25[OH] D ) before they were co-cultured with autologous memory CD4 T cells. Supernatants were harvested for cytokine analysis on Day 5 of co-culture, and intracellular cytokine staining was performed on Day 7. UPM-primed DCs increased the proportion of memory CD4 T cells expressing the T helper 17 cell (Th17)-associated cytokines IL-17A, IL-17F, and IL-22, as well as IFN-γ, granulocyte-macrophage colony-stimulating factor, and granzyme B. Notably, a large proportion of the UPM-driven IL-17A cells co-expressed these cytokines, but not IL-10, indicative of a proinflammatory Th17 profile. UPM-treated DCs expressed elevated levels of il23 mRNA and increased secretion of IL-23p40. Neutralization of IL-23 in culture reduced the frequency of IL-17A IFN-γ cells without affecting cell proliferation. 1,25(OH) D counteracted the UPM-driven DC maturation and inhibited the frequency of IL-17A IFN-γ cells, most prominently when DCs were co-treated with the corticosteroid dexamethasone, while maintaining antiinflammatory IL-10 synthesis. These data indicate that UPM might promote an inflammatory milieu in part by inducing an IL-23-driven proinflammatory Th17 response. Restoring vitamin D sufficiency may counteract these UPM-driven effects without obliterating important homeostatic immune functions.
[Mh] Termos MeSH primário: Cidades
Interferon gama/metabolismo
Interleucina-17/metabolismo
Interleucina-23/metabolismo
Material Particulado/toxicidade
Vitamina D/farmacologia
[Mh] Termos MeSH secundário: Calcitriol/farmacologia
Diferenciação Celular/efeitos dos fármacos
Células Dendríticas/efeitos dos fármacos
Células Dendríticas/metabolismo
Dexametasona/farmacologia
Seres Humanos
Células Mieloides/efeitos dos fármacos
Células Mieloides/metabolismo
Fenótipo
Células Th17/imunologia
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IL17A protein, human); 0 (Interleukin-17); 0 (Interleukin-23); 0 (Particulate Matter); 1406-16-2 (Vitamin D); 7S5I7G3JQL (Dexamethasone); 82115-62-6 (Interferon-gamma); FXC9231JVH (Calcitriol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2016-0409OC


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[PMID]:29324844
[Au] Autor:Barakat DJ; Suresh R; Barberi T; Pienta KJ; Simons BW; Friedman AD
[Ad] Endereço:Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
[Ti] Título:Absence of myeloid Klf4 reduces prostate cancer growth with pro-atherosclerotic activation of tumor myeloid cells and infiltration of CD8 T cells.
[So] Source:PLoS One;13(1):e0191188, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The microenvironment of prostate cancer often includes abundant tumor-associated macrophages (TAMs), with their acquisition of an M2 phenotype correlating with local aggressiveness and metastasis. Tumor-derived M-CSF contributes to TAM M2 polarization, and M-CSF receptor inhibition slows prostate cancer growth in model systems. As additional cytokines can direct TAM M2 polarization, targeting downstream transcription factors could avoid resistance. Klf4 and C/EBPß each contribute to monocyte development, and reduced expression of macrophage Klf4 or C/EBPß favors their adoption of a pro-inflammatory M1 state. We find that a Hi-Myc C57BL/6 prostate cancer line grows more slowly in syngeneic Klf4(f/f);Lys-Cre compared with Klf4(f/f) mice when inoculated subcutaneously, but grows equally rapidly in C/EBPß(f/f);Lys-Cre and C/EBPß(f/f) hosts. In the absence of myeloid Klf4, TAMs have reduced expression of surface mannose receptor and Fizz1 mRNA, both M2 markers. Global gene expression analysis further revealed activation of pro-inflammatory, pro-atherosclerotic pathways. Analysis of tumor-infiltrating lymphocytes (TILs) demonstrated markedly increased activated CD8 T cell numbers, and CD8 T cell depletion obviated the inhibitory effect of myeloid Klf4 deletion on prostate cancer growth. These findings suggest that reducing expression or activity of the Klf4 transcription factor in tumor myeloid cells may contribute to prostate cancer therapy.
[Mh] Termos MeSH primário: Fatores de Transcrição Kruppel-Like/deficiência
Neoplasias da Próstata/metabolismo
Neoplasias da Próstata/patologia
[Mh] Termos MeSH secundário: Animais
Aterosclerose/etiologia
Proteína beta Intensificadora de Ligação a CCAAT/deficiência
Proteína beta Intensificadora de Ligação a CCAAT/genética
Antígeno CD11c/metabolismo
Linfócitos T CD8-Positivos/imunologia
Linfócitos T CD8-Positivos/patologia
Linhagem Celular Tumoral
Fatores de Transcrição Kruppel-Like/genética
Lectinas Tipo C/metabolismo
Linfócitos do Interstício Tumoral
Macrófagos/imunologia
Macrófagos/metabolismo
Macrófagos/patologia
Masculino
Lectinas de Ligação a Manose/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Células Mieloides/imunologia
Células Mieloides/metabolismo
Células Mieloides/patologia
Neoplasias da Próstata/genética
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA Neoplásico/genética
RNA Neoplásico/metabolismo
Receptores de Superfície Celular/metabolismo
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (CCAAT-Enhancer-Binding Protein-beta); 0 (CD11c Antigen); 0 (GKLF protein); 0 (Kruppel-Like Transcription Factors); 0 (Lectins, C-Type); 0 (Mannose-Binding Lectins); 0 (RNA, Messenger); 0 (RNA, Neoplasm); 0 (Receptors, Cell Surface); 0 (mannose receptor)
[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:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191188


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[PMID]:29274779
[Au] Autor:Ishibashi T; Yokota T; Satoh Y; Ichii M; Sudo T; Doi Y; Ueda T; Nagate Y; Hamanaka Y; Tanimura A; Ezoe S; Shibayama H; Oritani K; Kanakura Y
[Ad] Endereço:Department of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan; Department of Vascular Physiology, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka 565-8565, Japan.
[Ti] Título:Identification of MS4A3 as a reliable marker for early myeloid differentiation in human hematopoiesis.
[So] Source:Biochem Biophys Res Commun;495(3):2338-2343, 2018 01 15.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Information of myeloid lineage-related antigen on hematopoietic stem/progenitor cells (HSPCs) is important to clarify the mechanisms regulating hematopoiesis, as well as for the diagnosis and treatment of myeloid malignancies. We previously reported that special AT-rich sequence binding protein 1 (SATB1), a global chromatin organizer, promotes lymphoid differentiation from HSPCs. To search a novel cell surface molecule discriminating early myeloid and lymphoid differentiation, we performed microarray analyses comparing SATB1-overexpressed HSPCs with mock-transduced HSPCs. The results drew our attention to membrane-spanning 4-domains, subfamily A, member 3 (Ms4a3) as the most downregulated molecule in HSPCs with forced overexpression of SATB1. Ms4a3 expression was undetectable in hematopoietic stem cells, but showed a concomitant increase with progressive myeloid differentiation, whereas not only lymphoid but also megakaryocytic-erythrocytic progenitors were entirely devoid of Ms4a3 expression. Further analysis revealed that a subset of CD34 CD38 CD33 progenitor population in human adult bone marrow expressed MS4A3, and those MS4A3 progenitors only produced granulocyte/macrophage colonies, losing erythroid colony- and mixed colony-forming capacity. These results suggest that cell surface expression of MS4A3 is useful to distinguish granulocyte/macrophage lineage-committed progenitors from other lineage-related ones in early human hematopoiesis. In conclusion, MS4A3 is useful to monitor early stage of myeloid differentiation in human hematopoiesis.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/metabolismo
Hematopoese/fisiologia
Células-Tronco Hematopoéticas/metabolismo
Proteínas de Membrana/metabolismo
Células Mieloides/citologia
Células Mieloides/metabolismo
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Diferenciação Celular
Células Cultivadas
Células-Tronco Hematopoéticas/citologia
Seres Humanos
Camundongos
Reprodutibilidade dos Testes
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cell Cycle Proteins); 0 (MS4A3 protein, human); 0 (Membrane Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171225
[St] Status:MEDLINE


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[PMID]:29324769
[Au] Autor:Meers GK; Bohnenberger H; Reichardt HM; Lühder F; Reichardt SD
[Ad] Endereço:Institute for Cellular and Molecular Immunology, University Medical Center Goettingen, Göttingen, Germany.
[Ti] Título:Impaired resolution of DSS-induced colitis in mice lacking the glucocorticoid receptor in myeloid cells.
[So] Source:PLoS One;13(1):e0190846, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammatory bowel disease (IBD) is a highly prevalent intestinal disorder for which no cure exists. Currently, the standard first-line treatment of IBD consists of systemic glucocorticoid (GC) application, even though therapy can be complicated by unresponsiveness or adverse effects. In view of the importance of macrophages and neutrophils for the pathogenesis of IBD we set out to define the relevance of these cell types as targets of GC using the mouse model of DSS-induced colitis. We found that the disease did not resolve in GRlysM mice lacking the GC receptor (GR) in myeloid cells after removal of the chemical insult. While clinical symptoms and tissue damage in the colon ameliorated again in GRflox mice, the disease further aggravated in GRlysM littermates. The observed difference coincided with an increased abundance of macrophages in inflammatory infiltrates in the colon of mutant mice whereas neutrophil and T cell numbers were similar. Concomitantly, systemic IL-6 secretion and mRNA levels of pro-inflammatory cytokines in the colon were elevated in GRlysM mice and gene expression of scavenger receptors and IL-10 was diminished. Taken together, our results reveal an important role of myeloid cells as targets of GC in DSS-induced colitis and probably in IBD in humans as well.
[Mh] Termos MeSH primário: Colite/imunologia
Células Mieloides/imunologia
Receptores de Glucocorticoides/deficiência
[Mh] Termos MeSH secundário: Animais
Colite/patologia
Colo/imunologia
Colo/patologia
Sulfato de Dextrana
Modelos Animais de Doenças
Interleucina-10/metabolismo
Interleucina-6/secreção
Mucosa Intestinal/imunologia
Mucosa Intestinal/patologia
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Células Mieloides/patologia
RNA Mensageiro/metabolismo
Receptores de Glucocorticoides/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL10 protein, mouse); 0 (Interleukin-6); 0 (RNA, Messenger); 0 (Receptors, Glucocorticoid); 0 (interleukin-6, mouse); 130068-27-8 (Interleukin-10); 9042-14-2 (Dextran Sulfate)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190846


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[PMID]:27770461
[Au] Autor:Piao X; Yamazaki S; Komazawa-Sakon S; Miyake S; Nakabayashi O; Kurosawa T; Mikami T; Tanaka M; Van Rooijen N; Ohmuraya M; Oikawa A; Kojima Y; Kakuta S; Uchiyama Y; Tanaka M; Nakano H
[Ad] Endereço:Department of Biochemistry, Toho University School of Medicine, Tokyo, Japan.
[Ti] Título:Depletion of myeloid cells exacerbates hepatitis and induces an aberrant increase in histone H3 in mouse serum.
[So] Source:Hepatology;65(1):237-252, 2017 01.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tissue-resident macrophages and bone marrow (BM)-derived monocytes play a crucial role in the maintenance of tissue homeostasis; however, their contribution to recovery from acute tissue injury is not fully understood. To address this issue, we generated an acute murine liver injury model using hepatocyte-specific Cflar-deficient (Cflar ) mice. Cellular FLICE-inhibitory protein expression was down-regulated in Cflar-deficient hepatocytes, which thereby increased susceptibility of hepatocytes to death receptor-induced apoptosis. Cflar mice developed acute hepatitis and recovered with clearance of apoptotic hepatocytes at 24 hours after injection of low doses of tumor necrosis factor α (TNFα), which could not induce hepatitis in wild-type (WT) mice. Depletion of Kupffer cells (KCs) by clodronate liposomes did not impair clearance of dying hepatocytes or exacerbate hepatitis in Cflar mice. To elucidate the roles of BM-derived monocytes and neutrophils in clearance of apoptotic hepatocytes, we examined the effect of depletion of these cells on TNFα-induced hepatitis in Cflar mice. We reconstituted Cflar mice with BM cells from transgenic mice in which human diphtheria toxin receptor (DTR) was expressed under control of the lysozyme M (LysM) promoter. TNFα-induced infiltration of myeloid cells, including monocytes and neutrophils, was completely ablated in LysM-DTR BM-reconstituted Cflar mice pretreated with diphtheria toxin, whereas KCs remained present in the livers. Under these experimental conditions, LysM-DTR BM-reconstituted Cflar mice rapidly developed severe hepatitis and succumbed within several hours of TNFα injection. We found that serum interleukin-6 (IL-6), TNFα, and histone H3 were aberrantly increased in LysM-DTR BM-reconstituted, but not in WT BM-reconstituted, Cflar mice following TNFα injection. CONCLUSION: These findings indicate an unexpected role of myeloid cells in decreasing serum IL-6, TNFα, and histone H3 levels via the suppression of TNFα-induced hepatocyte apoptosis. (Hepatology 2017;65:237-252).
[Mh] Termos MeSH primário: Hepatite/sangue
Hepatite/etiologia
Histonas/sangue
Células Mieloides/fisiologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Progressão da Doença
Hepatócitos
Macrófagos do Fígado
Camundongos
Camundongos Transgênicos
Fator de Necrose Tumoral alfa/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Histones); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180121
[Lr] Data última revisão:
180121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1002/hep.28878


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[PMID]:29261815
[Au] Autor:Bäcker V; Cheung FY; Siveke JT; Fandrey J; Winning S
[Ad] Endereço:Institut für Physiologie, Universität Duisburg-Essen, Essen, Germany.
[Ti] Título:Knockdown of myeloid cell hypoxia-inducible factor-1α ameliorates the acute pathology in DSS-induced colitis.
[So] Source:PLoS One;12(12):e0190074, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammation and hypoxia are hallmarks of inflammatory bowel disease. Low oxygen levels activate hypoxia-inducible factors as central transcriptional regulators of cellular responses to hypoxia, particularly in myeloid cells where hypoxia-inducible factors control immune cell function and survival. Still, the role of myeloid hypoxia-inducible factor-1 during inflammatory bowel disease remains poorly defined. We therefore investigated the role of hypoxia-inducible factor-1 for myeloid cell function and immune response during colitis. Experimental colitis was induced by administration of 2.5% dextran sulfate sodium to mice with a conditional knockout of hypoxia-inducible factor-1α in myeloid cells and their wild type siblings. Murine colon tissue was examined by histologic analysis, immunohistochemistry, and quantitative polymerase chain reaction. Induction of experimental colitis increased levels of hypoxia and accumulation of hypoxia-inducible factor-1α positive cells in colon tissue of both treated groups. Myeloid hypoxia-inducible factor-1α knockout reduced weight loss and disease activity index when compared to wild type mice. Knockout mice displayed less infiltration of macrophages into intestinal mucosa and reduced mRNA expression of markers for dendritic cells and interleukin-17 secreting T helper cells. Expression of inflammatory and anti-inflammatory cytokines also showed a reduced and delayed induction in myeloid hypoxia-inducible factor-1α knockout mice. Our results show a disease promoting role of myeloid hypoxia-inducible factor-1 during intestinal inflammation. This might result from a hypoxia-inducible factor-1 dependent increase in pro-inflammatory interleukin-17 secreting T helper cells in the absence of obvious changes in regulatory T cells. In contrast, knockout mice appear to shift the balance to anti-inflammatory signals and cells resulting in milder intestinal inflammation.
[Mh] Termos MeSH primário: Colite/induzido quimicamente
Colite/patologia
Técnicas de Silenciamento de Genes
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Células Mieloides/metabolismo
Células Mieloides/patologia
[Mh] Termos MeSH secundário: Animais
Hipóxia Celular
Polaridade Celular
Colite/complicações
Colo/patologia
Citocinas/genética
Citocinas/metabolismo
Sulfato de Dextrana
Feminino
Hipóxia/complicações
Hipóxia/metabolismo
Hipóxia/patologia
Inflamação/complicações
Inflamação/patologia
Macrófagos/patologia
Camundongos Endogâmicos C57BL
Camundongos Knockout
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Linfócitos T Reguladores/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (RNA, Messenger); 9042-14-2 (Dextran Sulfate)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190074


  9 / 4968 MEDLINE  
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[PMID]:29232557
[Au] Autor:Canli Ö; Nicolas AM; Gupta J; Finkelmeier F; Goncharova O; Pesic M; Neumann T; Horst D; Löwer M; Sahin U; Greten FR
[Ad] Endereço:Institute for Tumor Biology and Experimental Therapy, Georg-Speyer-Haus, 60596 Frankfurt/Main, Germany.
[Ti] Título:Myeloid Cell-Derived Reactive Oxygen Species Induce Epithelial Mutagenesis.
[So] Source:Cancer Cell;32(6):869-883.e5, 2017 Dec 11.
[Is] ISSN:1878-3686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Increased oxidative stress has been suggested to initiate and promote tumorigenesis by inducing DNA damage and to suppress tumor development by triggering apoptosis and senescence. The contribution of individual cell types in the tumor microenvironment to these contrasting effects remains poorly understood. We provide evidence that during intestinal tumorigenesis, myeloid cell-derived H O triggers genome-wide DNA mutations in intestinal epithelial cells to stimulate invasive growth. Moreover, increased reactive oxygen species (ROS) production in myeloid cells initiates tumor growth in various organs also in the absence of a carcinogen challenge in a paracrine manner. Our data identify an intricate crosstalk between myeloid cell-derived ROS molecules, oxidative DNA damage, and tumor necrosis factor α-mediated signaling to orchestrate a tumor-promoting microenvironment causing invasive cancer.
[Mh] Termos MeSH primário: Células Epiteliais/patologia
Mutagênese/fisiologia
Células Mieloides/metabolismo
Estresse Oxidativo/fisiologia
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Dano ao DNA/efeitos dos fármacos
Células Epiteliais/metabolismo
Peróxido de Hidrogênio/farmacologia
Camundongos
Camundongos Mutantes
Mutação
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Reactive Oxygen Species); BBX060AN9V (Hydrogen Peroxide)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171220
[Lr] Data última revisão:
171220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE


  10 / 4968 MEDLINE  
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[PMID]:28468987
[Au] Autor:Abrams SI
[Ad] Endereço:Department of Immunology, Roswell Park Cancer Institute, Buffalo, New York, USA scott.abrams@roswellpark.org.
[Ti] Título:Editorial: The rebirth of myeloid-derived suppressor cells: from adversary in cancer to ally in reproductive health.
[So] Source:J Leukoc Biol;101(5):1079, 2017 05.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Células Supressoras Mieloides
Saúde Reprodutiva
[Mh] Termos MeSH secundário: Seres Humanos
Células Mieloides
Neoplasias
[Pt] Tipo de publicação:EDITORIAL; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; COMMENT
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171215
[Lr] Data última revisão:
171215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.1CE1216-525R



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