Base de dados : MEDLINE
Pesquisa : D12.644.822.437 [Categoria DeCS]
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[PMID]:28393235
[Au] Autor:Gao F; Wang FG; Liu RR; Xue F; Zhang J; Xu GQ; Bi JH; Meng Z; Huo R
[Ad] Endereço:Department of Aesthetic, Plastic and Burn Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shangdong 250021, P.R. China.
[Ti] Título:Epigenetic silencing of miR-130a ameliorates hemangioma by targeting tissue factor pathway inhibitor 2 through FAK/PI3K/Rac1/mdm2 signaling.
[So] Source:Int J Oncol;50(5):1821-1831, 2017 May.
[Is] ISSN:1791-2423
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Hemangiomas are the most common vascular tumors that occur frequently in prematures and females. microRNA (miR)-130a is associated with the growth and invasion in many tumors, and its role in hemangiomas has not been addressed so far. The present study revealed that miR­130a was overexpressed in infantile hemangioma tissues compared with matched tumor-adjacent tissues. The inhibitor of miR-130a restrained cell growth and induced cell apoptosis in vitro. miR­130a inhibitor also induced a cell cycle arrest at G2/M phase. Further studies revealed that tissue factor pathway inhibitor 2 (TFPI2) was a novel miR-130a target, due to miR-130a bound directly to its 3'-untranslated region and miR-130a inhibitor enhanced the expression of TFPI2. Contrary to the effects of miR-130a inhibitor, TFPI2 siRNA strongly promoted cell growth and colony formation, whereas TFPI2 overexpression contributed to the suppressing effect of miR-130a inhibitor in cell viability. Furthermore, miR-130a inhibitor reduced the activation of focal adhesion kinase (FAK)/phosphoinositide 3-kinase (PI3K)/Rac1/anti-mouse double minute (mdm2) pathway proteins, inhibited the expression and nuclear translocation of mdm2. Moreover, FAK overexpression prevented miR-130a inhibitor-induced cell cycle arrest and decrease of cell viability. In vivo experiments, miR-130a inhibition effectively suppressed the tumor growth, restrained angiogenesis by decreasing the expression of angiogenesis markers and the percentage of CD31+ and CD34+. Taken together, our research indicated that miR-130a functions as an oncogene by targeting TFPI2, miR-130a inhibition reduced the growth and angiogenesis of hemangioma by inactivating the FAK/PI3K/Rac1/mdm2 pathway. Thus, miR-130a may serve as a potential therapeutic strategy for the treatment of hemangioma.
[Mh] Termos MeSH primário: Epigênese Genética/genética
Glicoproteínas/biossíntese
Hemangioma/genética
MicroRNAs/genética
Neovascularização Patológica/genética
[Mh] Termos MeSH secundário: Animais
Apoptose/genética
Proliferação Celular/genética
Sobrevivência Celular/genética
Elafina/genética
Feminino
Quinase 1 de Adesão Focal/genética
Regulação Neoplásica da Expressão Gênica
Glicoproteínas/genética
Hemangioma/patologia
Seres Humanos
Camundongos
MicroRNAs/biossíntese
Neovascularização Patológica/patologia
Proteínas Proto-Oncogênicas c-mdm2/genética
Transdução de Sinais
Ensaios Antitumorais Modelo de Xenoenxerto
Proteínas rac1 de Ligação ao GTP/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Elafin); 0 (Glycoproteins); 0 (MIRN130 microRNA, human); 0 (MicroRNAs); 0 (PI3 protein, human); 0 (RAC1 protein, human); 0 (tissue-factor-pathway inhibitor 2); EC 2.3.2.27 (MDM2 protein, human); EC 2.3.2.27 (Proto-Oncogene Proteins c-mdm2); EC 2.7.10.2 (Focal Adhesion Kinase 1); EC 2.7.10.2 (PTK2 protein, human); EC 3.6.5.2 (rac1 GTP-Binding Protein)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170720
[Lr] Data última revisão:
170720
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE
[do] DOI:10.3892/ijo.2017.3943


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[PMID]:28350788
[Au] Autor:Naito S; Makhov P; Astsaturov I; Golovine K; Tulin A; Kutikov A; Uzzo RG; Kolenko VM
[Ad] Endereço:Cancer Biology Program, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
[Ti] Título:LDL cholesterol counteracts the antitumour effect of tyrosine kinase inhibitors against renal cell carcinoma.
[So] Source:Br J Cancer;116(9):1203-1207, 2017 Apr 25.
[Is] ISSN:1532-1827
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Treatment with tyrosine kinase inhibitors (TKIs) significantly improves survival of patients with renal cell carcinoma (RCC). However, about one-quarter of the RCC patients are primarily refractory to treatment with TKIs. METHODS: We examined viability of RCC and endothelial cells treated with low-density lipoprotein (LDL) and/or TKIs. Next, we validated the potential role of PI3K/AKT signalling in LDL-mediated TKI resistance. Finally, we examined the effect of a high-fat/high-cholesterol diet on the response of RCC xenograft tumours to sunitinib. RESULTS: The addition of LDL cholesterol increases activation of PI3K/AKT signalling and compromises the antitumour efficacy of TKIs against RCC and endothelial cells. Furthermore, RCC xenograft tumours resist TKIs in mice fed a high-fat/high-cholesterol diet. CONCLUSIONS: The ability of renal tumours to maintain their cholesterol homoeostasis may be a critical component of TKI resistance in RCC patients.
[Mh] Termos MeSH primário: Carcinoma de Células Renais/tratamento farmacológico
Colesterol/metabolismo
Interações Medicamentosas/genética
Inibidores de Proteínas Quinases/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Carcinoma de Células Renais/metabolismo
Carcinoma de Células Renais/patologia
Linhagem Celular Tumoral
LDL-Colesterol/administração & dosagem
LDL-Colesterol/metabolismo
Interações Medicamentosas/etnologia
Elafina/genética
Células Endoteliais/efeitos dos fármacos
Células Endoteliais/metabolismo
Feminino
Seres Humanos
Indóis/administração & dosagem
Camundongos
Proteínas Proto-Oncogênicas c-akt/genética
Pirróis/administração & dosagem
Transdução de Sinais/efeitos dos fármacos
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholesterol, LDL); 0 (Elafin); 0 (Indoles); 0 (PI3 protein, human); 0 (Protein Kinase Inhibitors); 0 (Pyrroles); 97C5T2UQ7J (Cholesterol); EC 2.7.11.1 (AKT1 protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); V99T50803M (sunitinib)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE
[do] DOI:10.1038/bjc.2017.77


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[PMID]:28167848
[Au] Autor:Myntti T; Rahkonen L; Nupponen I; Pätäri-Sampo A; Tikkanen M; Sorsa T; Juhila J; Andersson S; Paavonen J; Stefanovic V
[Ad] Endereço:Department of Obstetrics and Gynecology, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.
[Ti] Título:Amniotic Fluid Infection in Preterm Pregnancies with Intact Membranes.
[So] Source:Dis Markers;2017:8167276, 2017.
[Is] ISSN:1875-8630
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:. Intra-amniotic infection (IAI) is a major cause of preterm labor and adverse neonatal outcome. We evaluated amniotic fluid (AF) proteolytic cascade forming biomarkers in relation to microbial invasion of the amniotic cavity (MIAC) and IAI in preterm pregnancies with intact membranes. . Amniocentesis was made to 73 women with singleton pregnancies; 27 with suspected IAI; and 46 controls. AF biomarkers were divided into three cascades: Cascade 1: matrix metalloproteinase-8 (MMP-8), MMP-9, myeloperoxidase (MPO), and interleukin-6; Cascade 2: neutrophil elastase (HNE), elafin, and MMP-9; Cascade 3: MMP-2, tissue inhibitor of matrix metalloproteinases-1 (TIMP-1), MMP-8/TIMP-1 molar ratio, and C-reactive protein (CRP). MMP-8 was measured by an immunoenzymometric assay and the others were measured by ELISA. Standard biochemical methods, molecular microbiology, and culture techniques were used. . MMP-8, MMP-9, MPO, elafin, and TIMP-1 concentrations were higher in IAI suspected cases compared to controls and also in IAI suspected cases with MIAC compared to those without MIAC when adjusted by gestational age at amniocentesis. All biomarkers except elafin and MMP-2 had the sensitivity of 100% with thresholds based on ROC-curve. Odd ratios of biomarkers for MIAC were 1.2-38 and 95% confidential intervals 1.0-353.6. . Neutrophil based AF biomarkers were associated with IAI and MIAC.
[Mh] Termos MeSH primário: Líquido Amniótico/metabolismo
Complicações Infecciosas na Gravidez/metabolismo
Nascimento Prematuro/metabolismo
Proteólise
[Mh] Termos MeSH secundário: Adulto
Líquido Amniótico/enzimologia
Líquido Amniótico/microbiologia
Biomarcadores/metabolismo
Estudos de Casos e Controles
Elafina/metabolismo
Feminino
Seres Humanos
Interleucina-6/metabolismo
Elastase de Leucócito/metabolismo
Metaloproteinases da Matriz/metabolismo
Peroxidase/metabolismo
Gravidez
Complicações Infecciosas na Gravidez/diagnóstico
Nascimento Prematuro/diagnóstico
Inibidor Tecidual de Metaloproteinase-1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Elafin); 0 (Interleukin-6); 0 (Tissue Inhibitor of Metalloproteinase-1); EC 1.11.1.7 (Peroxidase); EC 3.4.21.37 (Leukocyte Elastase); EC 3.4.24.- (Matrix Metalloproteinases)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170224
[Lr] Data última revisão:
170224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170208
[St] Status:MEDLINE
[do] DOI:10.1155/2017/8167276


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[PMID]:27893038
[Au] Autor:Basho RK; Gilcrease M; Murthy RK; Helgason T; Karp DD; Meric-Bernstam F; Hess KR; Herbrich SM; Valero V; Albarracin C; Litton JK; Chavez-MacGregor M; Ibrahim NK; Murray JL; Koenig KB; Hong D; Subbiah V; Kurzrock R; Janku F; Moulder SL
[Ad] Endereço:Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston.
[Ti] Título:Targeting the PI3K/AKT/mTOR Pathway for the Treatment of Mesenchymal Triple-Negative Breast Cancer: Evidence From a Phase 1 Trial of mTOR Inhibition in Combination With Liposomal Doxorubicin and Bevacizumab.
[So] Source:JAMA Oncol;3(4):509-515, 2017 Apr 01.
[Is] ISSN:2374-2445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: Triple-negative breast cancer (TNBC) classified by transcriptional profiling as the mesenchymal subtype frequently harbors aberrations in the phosphoinositide 3-kinase (PI3K) pathway, raising the possibility of targeting this pathway to enhance chemotherapy response. Up to 30% of mesenchymal TNBC can be classified histologically as metaplastic breast cancer, a chemorefractory group of tumors with a mixture of epithelial and mesenchymal components identifiable by light microscopy. While assays to identify mesenchymal TNBC are under development, metaplastic breast cancer serves as a clinically identifiable surrogate to evaluate potential regimens for mesenchymal TNBC. Objective: To assess safety and efficacy of mammalian target of rapamycin (mTOR) inhibition in combination with liposomal doxorubicin and bevacizumab in patients with advanced metaplastic TNBC. Design, Setting, and Participants: Phase 1 study with dose escalation and dose expansion at the University of Texas MD Anderson Cancer Center of patients with advanced metaplastic TNBC. Patients were enrolled from April 16, 2009, to November 4, 2014, and followed for outcomes with a cutoff date of November 1, 2015, for data analysis. Interventions: Liposomal doxorubicin, bevacizumab, and the mTOR inhibitors temsirolimus or everolimus using 21-day cycles. Main Outcomes and Measures: Safety and response. When available, archived tissue was evaluated for aberrations in the PI3K pathway. Results: Fifty-two women with metaplastic TNBC (median age, 58 years; range, 37-79 years) were treated with liposomal doxorubicin, bevacizumab, and temsirolimus (DAT) (N = 39) or liposomal doxorubicin, bevacizumab, and everolimus (DAE) (N = 13). The objective response rate was 21% (complete response = 4 [8%]; partial response = 7 [13%]) and 10 (19%) patients had stable disease for at least 6 months, for a clinical benefit rate of 40%. Tissue was available for testing in 43 patients, and 32 (74%) had a PI3K pathway aberration. Presence of PI3K pathway aberration was associated with a significant improvement in objective response rate (31% vs 0%; P = .04) but not clinical benefit rate (44% vs 45%; P > .99). Conclusions and Relevance: Using metaplastic TNBC as a surrogate for mesenchymal TNBC, DAT and DAE had notable activity in mesenchymal TNBC. Objective response was limited to patients with PI3K pathway aberration. A randomized trial should be performed to test DAT and DAE for metaplastic TNBC, as well as nonmetaplastic, mesenchymal TNBC, especially when PI3K pathway aberrations are identified.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Bevacizumab/administração & dosagem
Doxorrubicina/análogos & derivados
Neoplasias de Mama Triplo Negativas/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Idoso
Bevacizumab/efeitos adversos
Doxorrubicina/administração & dosagem
Doxorrubicina/efeitos adversos
Elafina/metabolismo
Everolimo/administração & dosagem
Everolimo/efeitos adversos
Feminino
Seres Humanos
Estimativa de Kaplan-Meier
Meia-Idade
Polietilenoglicóis/administração & dosagem
Polietilenoglicóis/efeitos adversos
Modelos de Riscos Proporcionais
Inibidores de Proteínas Quinases/administração & dosagem
Inibidores de Proteínas Quinases/efeitos adversos
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
Sirolimo/administração & dosagem
Sirolimo/efeitos adversos
Sirolimo/análogos & derivados
Serina-Treonina Quinases TOR/metabolismo
Neoplasias de Mama Triplo Negativas/patologia
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Elafin); 0 (PI3 protein, human); 0 (Protein Kinase Inhibitors); 0 (liposomal doxorubicin); 2S9ZZM9Q9V (Bevacizumab); 30IQX730WE (Polyethylene Glycols); 624KN6GM2T (temsirolimus); 80168379AG (Doxorubicin); 9HW64Q8G6G (Everolimus); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); W36ZG6FT64 (Sirolimus)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170421
[Lr] Data última revisão:
170421
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161129
[St] Status:MEDLINE
[do] DOI:10.1001/jamaoncol.2016.5281


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[PMID]:27698252
[Au] Autor:Zhong QQ; Wang X; Li YF; Peng LJ; Jiang ZS
[Ad] Endereço:1 Department of Cardiology, Xiangya Hospital, Central South University, Changsha 410008, China.
[Ti] Título:Secretory leukocyte protease inhibitor promising protective roles in obesity-associated atherosclerosis.
[So] Source:Exp Biol Med (Maywood);242(3):250-257, 2017 Feb.
[Is] ISSN:1535-3699
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Secretory leukocyte protease inhibitor (SLPI), a serine protease inhibitor, which was most commonly examined in mucosal fluids such as saliva, is a versatile molecule and plays non-redundant roles. In addition to its anti-protease activity, SLPI has been shown to express anti-bacterial, anti-viral, anti-fungal, and anti-inflammatory properties as well as participating in innate and adaptive immune responses, most of which has been well documented. Recently, it is reported that SLPI is expressed in adipocytes and adipose tissue where it could play an important feedback role in the resolution of inflammation. Furthermore, circulating SLPI has been shown to correlate with progressive metabolic dysfunction. Moreover, adenoviral gene delivery of elafin and SLPI attenuates nuclear factor-κB-dependent inflammatory responses of human endothelial cells and macrophages to atherogenic stimuli. This review contributes to unraveling the protective role of SLPI in obesity-related atherosclerosis development, and the potential role in preventing arterial plaque rupture.
[Mh] Termos MeSH primário: Anti-Inflamatórios/metabolismo
Antioxidantes/metabolismo
Aterosclerose/patologia
Obesidade/patologia
Placa Aterosclerótica/patologia
Inibidor Secretado de Peptidases Leucocitárias/metabolismo
[Mh] Termos MeSH secundário: Adipócitos/metabolismo
Tecido Adiposo/citologia
Tecido Adiposo/metabolismo
Aterosclerose/complicações
Elafina/genética
Elafina/metabolismo
Seres Humanos
Inflamação/prevenção & controle
Obesidade/etiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antioxidants); 0 (Elafin); 0 (PI3 protein, human); 0 (SLPI protein, human); 0 (Secretory Leukocyte Peptidase Inhibitor)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161005
[St] Status:MEDLINE
[do] DOI:10.1177/1535370216672747


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[PMID]:27580179
[Au] Autor:Stalberg C; Noda N; Polettini J; Jacobsson B; Menon R
[Ti] Título:Anti-inflammatory Elafin in human fetal membranes.
[So] Source:J Perinat Med;45(2):237-244, 2017 Feb 01.
[Is] ISSN:1619-3997
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Elafin is a low molecular weight protein with antileukoproteinase, anti-inflammatory, antibacterial and immunomodulating properties. The profile of Elafin in fetal membranes is not well characterized. This study determined the changes in Elafin expression and concentration in human fetal membrane from patients with preterm prelabor rupture of membranes (PPROM) and in vitro in response to intra-amniotic polymicrobial pathogens. METHOD: Elafin messenger RNA (mRNA) expressions were studied in fetal membranes from PPROM, normal term as well as in normal term not in labor membranes in an organ explant system treated (24 h) with lipopolysaccharide (LPS), using quantitative reverse transcription-polymerase chain reaction (RT-PCR). Enzyme-linked immunosorbent assay (ELISA) measured Elafin concentrations in culture supernatants from tissues treated with LPS and polybacterial combinations of heat-inactivated Mycoplasma hominis (MH), Ureaplasma urealyticum (UU) and Gardnerella vaginalis (GV). RESULTS: Elafin mRNA expression in fetal membranes from women with PPROM was significantly higher compared to women who delivered at term after normal pregnancy (5.09±3.50 vs. 11.71±2.21; P<0.05). In vitro, LPS-stimulated membranes showed a significantly increased Elafin m-RNA expression (P<0.05). However, the protein levels after LPS stimulation was not changed. Similarly, polymicrobial-treated fetal membranes also showed no changes in Elafin protein concentrations compared to untreated controls. CONCLUSION: Higher Elafin expression in PPROM fetal membranes suggests a host response to an inflammatory pathology. However, lack of Elafin response to LPS and polymicrobial treatment is indicative of the minimal anti-inflammatory impact of this molecule in fetal membranes.
[Mh] Termos MeSH primário: Elafina/metabolismo
Membranas Extraembrionárias/metabolismo
Ruptura Prematura de Membranas Fetais/metabolismo
[Mh] Termos MeSH secundário: Feminino
Interações Hospedeiro-Patógeno
Seres Humanos
Técnicas In Vitro
Inflamação/metabolismo
Lipopolissacarídeos
Técnicas de Cultura de Órgãos
Gravidez
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Elafin); 0 (Lipopolysaccharides); 0 (PI3 protein, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160901
[St] Status:MEDLINE


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[PMID]:27579858
[Au] Autor:Rodriguez-Garcia M; Shen Z; Barr FD; Boesch AW; Ackerman ME; Kappes JC; Ochsenbauer C; Wira CR
[Ad] Endereço:Department of Physiology and Neurobiology, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire, USA.
[Ti] Título:Dendritic cells from the human female reproductive tract rapidly capture and respond to HIV.
[So] Source:Mucosal Immunol;10(2):531-544, 2017 Mar.
[Is] ISSN:1935-3456
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dendritic cells (DCs) throughout the female reproductive tract (FRT) were examined for phenotype, HIV capture ability and innate anti-HIV responses. Two main CD11c DC subsets were identified: CD11b and CD11b DCs. CD11b CD14 DCs were the most abundant throughout the tract. A majority of CD11c CD14 cells corresponded to CD1c myeloid DCs, whereas the rest lacked CD1c and CD163 expression (macrophage marker) and may represent monocyte-derived cells. In addition, we identified CD103 DCs, located exclusively in the endometrium, whereas DC-SIGN DCs were broadly distributed throughout the FRT. Following exposure to GFP-labeled HIV particles, CD14 DC-SIGN as well as CD14 DC-SIGN cells captured virus, with ∼30% of these cells representing CD1c myeloid DCs. CD103 DCs lacked HIV capture ability. Exposure of FRT DCs to HIV induced secretion of CCL2, CCR5 ligands, interleukin (IL)-8, elafin, and secretory leukocyte peptidase inhibitor (SLPI) within 3 h of exposure, whereas classical pro-inflammatory molecules did not change and interferon-α2 and IL-10 were undetectable. Furthermore, elafin and SLPI upregulation, but not CCL5, were suppressed by estradiol pre-treatment. Our results suggest that specific DC subsets in the FRT have the potential for capture and dissemination of HIV, exert antiviral responses and likely contribute to the recruitment of HIV-target cells through the secretion of innate immune molecules.
[Mh] Termos MeSH primário: Células Dendríticas/imunologia
Genitália Feminina/imunologia
Infecções por HIV/imunologia
HIV/imunologia
Imunidade Inata
[Mh] Termos MeSH secundário: Antígeno CD11c/metabolismo
Moléculas de Adesão Celular/metabolismo
Células Cultivadas
Quimiocina CCL2/metabolismo
Células Dendríticas/virologia
Elafina/metabolismo
Estradiol/farmacologia
Feminino
HIV/patogenicidade
Infecções por HIV/transmissão
Seres Humanos
Interleucina-8/metabolismo
Lectinas Tipo C/metabolismo
Receptores de Lipopolissacarídeos/metabolismo
Fagocitose
Receptores CCR5/metabolismo
Receptores de Superfície Celular/metabolismo
Inibidor Secretado de Peptidases Leucocitárias/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCR5 protein, human); 0 (CD11c Antigen); 0 (Cell Adhesion Molecules); 0 (Chemokine CCL2); 0 (DC-specific ICAM-3 grabbing nonintegrin); 0 (Elafin); 0 (Interleukin-8); 0 (Lectins, C-Type); 0 (Lipopolysaccharide Receptors); 0 (Receptors, CCR5); 0 (Receptors, Cell Surface); 0 (SLPI protein, human); 0 (Secretory Leukocyte Peptidase Inhibitor); 4TI98Z838E (Estradiol)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160901
[St] Status:MEDLINE
[do] DOI:10.1038/mi.2016.72


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[PMID]:27636701
[Au] Autor:Kalams SA; Rogers LM; Smith RM; Barnett L; Crumbo K; Sumner S; Prashad N; Rybczyk K; Milne G; Dowd SE; Chong E; Winikoff B; Aronoff DM
[Ad] Endereço:a Division of Infectious Diseases, Department of Medicine , Vanderbilt University Medical Center , Nashville , TN , USA.
[Ti] Título:Neither vaginal nor buccal administration of 800 µg misoprostol alters mucosal and systemic immune activation or the cervicovaginal microbiome: a pilot study.
[So] Source:Eur J Contracept Reprod Health Care;21(6):436-442, 2016 Dec.
[Is] ISSN:1473-0782
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: The aim of the study was to assess the extent to which misoprostol alters mucosal or systemic immune responses following either buccal or vaginal administration. METHODS: This was a prospective, crossover pilot study of 15 healthy, reproductive-age women. Women first received 800 µg misoprostol either via buccal or vaginal administration and were crossed over 1 month later to receive the drug via the other route. Cervicovaginal lavage samples, cervical Cytobrush samples, cervicovaginal swabs, urine and blood were obtained immediately prior to drug administration and the following day. Parameters assessed included urine and cervicovaginal misoprostol levels, whole blood cytokine responses (by ELISA) to immune stimulation with lipopolysaccharide, peripheral blood and cervical lymphocyte phenotyping by flow cytometry, cervicovaginal antimicrobial peptide measurement by ELISA and vaginal microbial ecology assessment by 16S rRNA sequencing. RESULTS: Neither buccal nor vaginal misoprostol significantly altered local or systemic immune and microbiological parameters. CONCLUSION: In this pilot study, we did not observe significant alteration of mucosal or systemic immunology or vaginal microbial ecology 1 day after drug administration following either the buccal or vaginal route.
[Mh] Termos MeSH primário: Abortivos não Esteroides/farmacologia
Colo do Útero
Misoprostol/farmacologia
Vagina
[Mh] Termos MeSH secundário: Abortivos não Esteroides/administração & dosagem
Administração Bucal
Administração Intravaginal
Colo do Útero/efeitos dos fármacos
Colo do Útero/imunologia
Colo do Útero/microbiologia
Estudos Cross-Over
Elafina/sangue
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Sistema Imunitário/efeitos dos fármacos
Linfócitos/efeitos dos fármacos
Microbiota
Misoprostol/administração & dosagem
Projetos Piloto
Estados Unidos
Vagina/efeitos dos fármacos
Vagina/imunologia
Vagina/microbiologia
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Abortifacient Agents, Nonsteroidal); 0 (Elafin); 0 (PI3 protein, human); 0E43V0BB57 (Misoprostol)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170909
[Lr] Data última revisão:
170909
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160917
[St] Status:MEDLINE


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[PMID]:27393267
[Au] Autor:Hughes BL; Dutt R; Raker C; Barthelemy M; Rossoll RM; Ramratnam B; Wira CR; Cu-Uvin S
[Ad] Endereço:Department of Obstetrics and Gynecology, Division of Maternal Fetal Medicine, Warren Alpert Medical School of Brown University, Women and Infants Hospital, Providence, RI. Electronic address: bhughes@wihri.org.
[Ti] Título:The impact of pregnancy on anti-HIV activity of cervicovaginal secretions.
[So] Source:Am J Obstet Gynecol;215(6):748.e1-748.e12, 2016 Dec.
[Is] ISSN:1097-6868
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Mucosal immunity of the female genital tract plays a critical role in defense against sexually transmitted infections like HIV. Pregnancy is associated with both structural and immunologic alterations in the genital mucosa, but the impact of these changes on its ability to suppress HIV infection is unknown. Current epidemiologic data are conflicting as to whether pregnancy increases the risk of HIV acquisition. OBJECTIVE: The purpose of this study was to define the association between antimicrobial peptides and chemokines in cervicovaginal secretions and in vitro HIV infectivity among pregnant and nonpregnant women. STUDY DESIGN: Forty pregnant and 37 nonpregnant women were enrolled in a prospective longitudinal cohort study at a single tertiary care women's hospital in Providence, RI. Cervicovaginal lavage was performed at each study visit. For pregnant women, study visits occurred once per trimester, and there was an optional postpartum visit. For nonpregnant women, study visits occurred across a single cycle that was timed to occur in the proliferative, ovulatory, and secretory phases based on the presumption of a regular menstrual cycle. The impact of cervicovaginal lavage on HIV infectivity was evaluated using a TZM-bl assay and compared between pregnant and nonpregnant women for each visit. The previously validated TZM-bl assay, which uses a luciferase reporting gene to indicate HIV infection of TZM-bl cells, was measured with a luminometer with higher relative light units that indicate greater levels of in vitro HIV infection. Immune mediators were measured with a multiplex bead assay. HIV infectivity and median concentration of each mediator were compared between pregnant and nonpregnant groups with the Wilcoxon rank sum test. RESULTS: Cervicovaginal fluid from pregnant and nonpregnant women significantly decreased HIV infectivity in both groups compared with positive control (virus only; P<.01), but infectivity was not different between groups (P≥.44). During the second and third trimesters, pregnant women experienced suppression of several cervicovaginal immune mediators that included human beta defensin-2; lactoferrin; macrophage inflammatory protein-3α; regulated on activation, normally T-cell expressed and secreted; and stromal cell-derived factor-1 (all P≤.05). The antimicrobial peptide elafin was significantly correlated with HIV infectivity in both groups across all visits, except at the postpartum visit in the pregnant group (n=16). Secretory leukocyte protease inhibitor also was correlated significantly with infectivity across all visits, but in nonpregnant women only (P≤.03). CONCLUSION: Cervicovaginal secretions from both pregnant and nonpregnant women contain immune mediators that are associated with HIV infectivity in an in vitro assay; however, infectivity was not different between pregnant and nonpregnant groups. If pregnant women are at increased risk for HIV infection, it is unlikely to be mediated by alterations in the effectiveness of these protective secretions.
[Mh] Termos MeSH primário: Colo do Útero/imunologia
Infecções por HIV/imunologia
HIV-1/imunologia
Imunidade nas Mucosas/imunologia
Gravidez/imunologia
Vagina/imunologia
[Mh] Termos MeSH secundário: Adulto
Estudos de Casos e Controles
Colo do Útero/secreção
Quimiocina CCL20/imunologia
Quimiocina CXCL12/imunologia
Elafina/imunologia
Feminino
Seres Humanos
Lactoferrina/imunologia
Estudos Longitudinais
Estudos Prospectivos
Inibidor Secretado de Peptidases Leucocitárias
Vagina/secreção
Ducha Vaginal
Adulto Jovem
beta-Defensinas/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CCL20); 0 (Chemokine CXCL12); 0 (Elafin); 0 (Secretory Leukocyte Peptidase Inhibitor); 0 (beta-Defensins); EC 3.4.21.- (Lactoferrin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170531
[Lr] Data última revisão:
170531
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160710
[St] Status:MEDLINE


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[PMID]:27235719
[Au] Autor:Estruch M; Sanchez-Quesada JL; Ordoñez-Llanos J; Benitez S
[Ad] Endereço:Biomedical Research Institute Sant Pau (IIB-Sant Pau), Barcelona, Spain, C/Sant Antoni M. Claret 167, 08025 Barcelona, Spain. Electronic address: mestruch@santpau.cat.
[Ti] Título:Inflammatory intracellular pathways activated by electronegative LDL in monocytes.
[So] Source:Biochim Biophys Acta;1861(9 Pt A):963-969, 2016 09.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Electronegative LDL (LDL(-)) is a plasma LDL subfraction that induces cytokine release in monocytes through toll-like receptor 4 (TLR4) activation. However, the intracellular pathways induced by LDL(-) downstream TLR4 activation are unknown. We aimed to identify the pathways activated by LDL(-) leading to cytokine release in monocytes. METHODS AND RESULTS: We determined LDL(-)-induced activation of several intracellular kinases in protein extracts from monocytes using a multikinase ELISA array. LDL(-) induced higher p38 mitogen-activated protein kinase (MAPK) phosphorylation than native LDL. This was corroborated by a specific cell-based assay and it was dependent on TLR4 and phosphoinositide 3-kinase (PI3k)/Akt pathway. P38 MAPK activation was involved in cytokine release promoted by LDL(-). A specific ELISA showed that LDL(-) activated cAMP response-element binding (CREB) in a p38 MAPK dependent manner. P38 MAPK was also involved in the nuclear factor kappa-B (NF-kB) and activating protein-1 (AP-1) activation by LDL(-). We found that NF-kB, AP-1 and CREB inhibitors decreased LDL(-)-induced cytokine release, mainly on MCP1, IL6 and IL10 release, respectively. CONCLUSIONS: LDL(-) promotes p38 MAPK phosphorylation through TLR4 and PI3k/Akt pathways. Phosphorylation of p38 MAPK is involved in NF-kB, AP-1 and CREB activation, leading to LDL(-)-induced cytokine release in monocytes.
[Mh] Termos MeSH primário: Lipoproteínas LDL/sangue
Monócitos/metabolismo
Receptor 4 Toll-Like/genética
Proteínas Quinases p38 Ativadas por Mitógeno/genética
[Mh] Termos MeSH secundário: AMP Cíclico/metabolismo
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/biossíntese
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/genética
Citocinas/biossíntese
Citocinas/genética
Elafina/genética
Seres Humanos
Lipoproteínas LDL/biossíntese
NF-kappa B/biossíntese
NF-kappa B/genética
Fosforilação
Proteínas Proto-Oncogênicas c-akt/genética
Transdução de Sinais
Fator de Transcrição AP-1/biossíntese
Fator de Transcrição AP-1/genética
Proteínas Quinases p38 Ativadas por Mitógeno/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CREB1 protein, human); 0 (Cyclic AMP Response Element-Binding Protein); 0 (Cytokines); 0 (Elafin); 0 (Lipoproteins, LDL); 0 (NF-kappa B); 0 (PI3 protein, human); 0 (TLR4 protein, human); 0 (Toll-Like Receptor 4); 0 (Transcription Factor AP-1); 0 (oxidized low density lipoprotein); E0399OZS9N (Cyclic AMP); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170830
[Lr] Data última revisão:
170830
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160529
[St] Status:MEDLINE



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