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[PMID]:28574259
[Au] Autor:Kozikowski AP; Onajole OK; Stec J; Dupont C; Viljoen A; Richard M; Chaira T; Lun S; Bishai W; Raj VS; Ordway D; Kremer L
[Ad] Endereço:Drug Discovery Program, Department of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, University of Illinois at Chicago , 833 South Wood Street, Chicago, Illinois 60612, United States.
[Ti] Título:Targeting Mycolic Acid Transport by Indole-2-carboxamides for the Treatment of Mycobacterium abscessus Infections.
[So] Source:J Med Chem;60(13):5876-5888, 2017 Jul 13.
[Is] ISSN:1520-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mycobacterium abscessus is a fast-growing, multidrug-resistant organism that has emerged as a clinically significant pathogen in cystic fibrosis (CF) patients. The intrinsic resistance of M. abscessus to most commonly available antibiotics seriously restricts chemotherapeutic options. Herein, we report the potent activity of a series of indolecarboxamides against M. abscessus. The lead compounds, 6 and 12, exhibited strong activity in vitro against a wide panel of M. abscessus isolates and in infected macrophages. High resistance levels to the indolecarboxamides appear to be associated with an A309P mutation in the mycolic acid transporter MmpL3. Biochemical analyses demonstrated that while de novo mycolic acid synthesis remained unaffected, the indolecarboxamides strongly inhibited the transport of trehalose monomycolate, resulting in the loss of trehalose dimycolate production and abrogating mycolylation of arabinogalactan. Our data introduce a hereto unexploited chemical structure class active against M. abscessus infections with promising translational development possibilities for the treatment of CF patients.
[Mh] Termos MeSH primário: Antibacterianos/química
Antibacterianos/farmacologia
Indóis/química
Indóis/farmacologia
Mycobacterium/efeitos dos fármacos
Ácidos Micólicos/metabolismo
[Mh] Termos MeSH secundário: Transporte Biológico/efeitos dos fármacos
Linhagem Celular
Fatores Corda/metabolismo
Seres Humanos
Testes de Sensibilidade Microbiana
Mycobacterium/metabolismo
Infecções por Mycobacterium/tratamento farmacológico
Infecções por Mycobacterium/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Cord Factors); 0 (Indoles); 0 (Mycolic Acids); 0 (trehalose monomycolate)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jmedchem.7b00582


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[PMID]:28165282
[Au] Autor:Hwang SA; Kruzel ML; Actor JK
[Ad] Endereço:a Department of Pathology and Laboratory Medicine, UTHealth McGovern Medical School, Houston, TX 77030, USA.
[Ti] Título:Oral recombinant human or mouse lactoferrin reduces Mycobacterium tuberculosis TDM induced granulomatous lung pathology.
[So] Source:Biochem Cell Biol;95(1):148-154, 2017 Feb.
[Is] ISSN:1208-6002
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:Trehalose 6'6-dimycolate (TDM) is the most abundant glycolipid on the cell wall of Mycobacterium tuberculosis (MTB). TDM is capable of inducing granulomatous pathology in mouse models that resembles those induced by MTB infection. Using the acute TDM model, this work investigates the effect of recombinant human and mouse lactoferrin to reduce granulomatous pathology. C57BL/6 mice were injected intravenously with TDM at a dose of 25 µg·mouse . At day 4 and 6, recombinant human or mouse lactoferrin (1 mg·(100 µL) ·mouse ) were delivered by gavage. At day 7 after TDM injection, mice were evaluated for lung pathology, cytokine production, and leukocyte populations. Mice given human or mouse lactoferrin had reduced production of IL-12p40 in their lungs. Mouse lactoferrin increased IL-6 and KC (CXCL1) in lung tissue. Increased numbers of macrophages were observed in TDM-injected mice given human or mouse lactoferrin. Granulomatous pathology, composed of mainly migrated leukocytes, was visually reduced in mice that received human or mouse lactoferrin. Quantitation of granulomatous pathology demonstrated a significant decrease in mice given human or mouse lactoferrin compared with TDM control mice. This report is the first to directly compare the immune modulatory effects of both heterologous recombinant human and homologous mouse lactoferrin on the development of TDM-induced granulomas.
[Mh] Termos MeSH primário: Fatores Corda/efeitos adversos
Granuloma/prevenção & controle
Lactoferrina/administração & dosagem
Pneumopatias/prevenção & controle
Proteínas Recombinantes/administração & dosagem
Tuberculose/prevenção & controle
[Mh] Termos MeSH secundário: Administração Oral
Animais
Fatores Corda/metabolismo
Citocinas/metabolismo
Feminino
Granuloma/induzido quimicamente
Granuloma/metabolismo
Granuloma/patologia
Seres Humanos
Pneumopatias/induzido quimicamente
Pneumopatias/metabolismo
Pneumopatias/patologia
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Mycobacterium tuberculosis/metabolismo
Tuberculose/metabolismo
Tuberculose/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cord Factors); 0 (Cytokines); 0 (LTF protein, human); 0 (Ltf protein, mouse); 0 (Recombinant Proteins); EC 3.4.21.- (Lactoferrin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170614
[Lr] Data última revisão:
170614
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170207
[St] Status:MEDLINE
[do] DOI:10.1139/bcb-2016-0061


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[PMID]:27743706
[Au] Autor:Hunter RL; Hwang SA; Jagannath C; Actor JK
[Ad] Endereço:Department of Pathology and Laboratory Medicine, University of Texas, Houston Medical School, MSB 2.136, 6431 Fannin, Houston, TX, 77030, USA. Electronic address: Robert.L.Hunter@UTH.TMC.EDU.
[Ti] Título:Cord factor as an invisibility cloak? A hypothesis for asymptomatic TB persistence.
[So] Source:Tuberculosis (Edinb);101S:S2-S8, 2016 Dec.
[Is] ISSN:1873-281X
[Cp] País de publicação:Scotland
[La] Idioma:eng
[Ab] Resumo:Mycobacterium tuberculosis (MTB) has long been known to persist in grossly normal tissues even in people with active lesions and granulomas in other parts of the body. We recently reported that post-primary TB begins as an asymptomatic infection that slowly progresses, accumulating materials for a massive necrotizing reaction that results in cavitation. This paper explores the possible roles of trehalose 6,6' dimycolate (TDM) or cord factor in the ability of MTB to persist in such lesions without producing inflammation. TDM is unique in that it has three distinct sets of biologic activities depending on its physical conformation. As a single molecule, TDM stimulates macrophage C-type lectin receptors including Mincle. TDM can also form three crystal like structures, cylindrical micelles, intercalated bilayer and monolayer, that have distinct non receptor driven activities that depend on modulation of interactions with water. In the monolayer form, TDM is highly toxic and destroys cells in minutes upon contact. The cylindrical micelles and an intercalated bilayer have surfaces composed entirely of trehalose which protect MTB from killing in macrophages. Here we review evidence that these trehalose surfaces bind water. We speculate that this immobilized water constituites of an "invisibility cloak" that facilitates the persistence of MTB in multiple cell types without producing inflammation, even in highly immune individuals.
[Mh] Termos MeSH primário: Fatores Corda/metabolismo
Macrófagos/microbiologia
Mycobacterium tuberculosis/metabolismo
Tuberculose/microbiologia
[Mh] Termos MeSH secundário: Animais
Doenças Assintomáticas
Seres Humanos
Lectinas Tipo C/metabolismo
Macrófagos/imunologia
Macrófagos/metabolismo
Mycobacterium tuberculosis/imunologia
Mycobacterium tuberculosis/patogenicidade
Receptores Imunológicos/metabolismo
Transdução de Sinais
Tuberculose/imunologia
Tuberculose/metabolismo
Água/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (CLEC4D protein, human); 0 (Cord Factors); 0 (Lectins, C-Type); 0 (Receptors, Immunologic); 059QF0KO0R (Water)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161017
[St] Status:MEDLINE


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[PMID]:27742461
[Au] Autor:Arora R; Armitige L; Wanger A; Hunter RL; Hwang SA
[Ad] Endereço:Department of Pathology and Laboratory Medicine, University of Kentucky, Lexington, KY, USA.
[Ti] Título:Association of pellicle growth morphological characteristics and clinical presentation of Mycobacterium tuberculosis isolates.
[So] Source:Tuberculosis (Edinb);101S:S63-S68, 2016 Dec.
[Is] ISSN:1873-281X
[Cp] País de publicação:Scotland
[La] Idioma:eng
[Ab] Resumo:Trehalose 6,6'dimycolate (TDM) is a glycolipid found in nearly pure form on the surface of virulent Mycobacterium tuberculosis (MTB). This manuscript investigated the production of TDM, growth rate and colony morphology of multiple strains of MTB, each of which had been isolated from both pulmonary (sputum) and extrapulmonary sites of multiple patients. Since sputum contains MTB primarily from cavities and extrapulmonary biopsies are typically granulomas, this provided an opportunity to compare the behavior of single strains of MTB that had been isolated from cavities and granulomas. The results demonstrated that MTB isolated from pulmonary sites produced more TDM (3.23 ± 1.75 µg TDM/mg MTB), grew more rapidly as thin spreading pellicles, demonstrated early cording, and climbed culture well walls. In contrast, extrapulmonary isolates produced less TDM (1.42 ± 0.58 µg TDM/mg MTB) (p < 0.001) and grew as discrete patches with little tendency to spread or climb. Both Beijing pulmonary isolates and the non-Beijing pulmonary isolates produced significantly more TDM (1.64 ± 0.46 µg TDM/mg MTB) and grew faster than the Beijing and non-Beijing extrapulmonary isolates (1.14 ± 0.63 µg TDM/mg MTB) (p < 0.001 and p < 0.005 respectively). These results indicate that MTB from pulmonary sites (cavities) grows faster and produces more TDM than strains isolated from extrapulmonary sites (granulomas). This report suggests a critical role for TDM in cavitary TB.
[Mh] Termos MeSH primário: Fatores Corda/metabolismo
Granuloma/microbiologia
Mycobacterium tuberculosis/metabolismo
Tuberculose Pulmonar/microbiologia
[Mh] Termos MeSH secundário: Biópsia
Seres Humanos
Mycobacterium tuberculosis/crescimento & desenvolvimento
Mycobacterium tuberculosis/isolamento & purificação
Mycobacterium tuberculosis/patogenicidade
Escarro/microbiologia
Fatores de Tempo
Virulência
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cord Factors)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161016
[St] Status:MEDLINE


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[PMID]:27164021
[Au] Autor:Mehta PK; Singh N; Dharra R; Dahiya B; Sharma S; Sheoran A; Gupta KB; Chaudhary D; Mehta N; Varma-Basil M
[Ad] Endereço:Centre for Biotechnology, Maharshi Dayanand University (MDU), Rohtak, 124001 Haryana, India. Electronic address: pkmehta3@hotmail.com.
[Ti] Título:Diagnosis of tuberculosis based on the detection of a cocktail of mycobacterial antigen 85B, ESAT-6 and cord factor by immuno-PCR.
[So] Source:J Microbiol Methods;127:24-7, 2016 08.
[Is] ISSN:1872-8359
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Attempts were made to enhance the sensitivity of immuno-PCR assay based on the detection of cocktail of mycobacterial antigen 85B (Rv1886c), ESAT-6 (Rv3875) and cord factor (trehalose 6,6'-dimycolate) in pulmonary and extrapulmonary TB patients. Detection of Ag85B was found to be superior to the detection of cocktail in TB patients.
[Mh] Termos MeSH primário: Antígenos de Bactérias/análise
Fatores Corda/análise
Reação em Cadeia da Polimerase/métodos
Tuberculose/diagnóstico
[Mh] Termos MeSH secundário: Antígenos de Bactérias/imunologia
Fatores Corda/imunologia
Imunoensaio/métodos
Tuberculose/microbiologia
Tuberculose Pulmonar/diagnóstico
Tuberculose Pulmonar/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, Bacterial); 0 (Cord Factors); 0 (ESAT-6 antigen, Mycobacterium leprae); 146045-22-9 (antigen 85B, Mycobacterium leprae)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160511
[St] Status:MEDLINE


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[PMID]:27089465
[Au] Autor:Lee WB; Kang JS; Choi WY; Zhang Q; Kim CH; Choi UY; Kim-Ha J; Kim YJ
[Ad] Endereço:Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, Republic of Korea.
[Ti] Título:Mincle-mediated translational regulation is required for strong nitric oxide production and inflammation resolution.
[So] Source:Nat Commun;7:11322, 2016 Apr 18.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In response to persistent mycobacteria infection, the host induces a granuloma, which often fails to eradicate bacteria and results in tissue damage. Diverse host receptors are required to control the formation and resolution of granuloma, but little is known concerning their regulatory interactions. Here we show that Mincle, the inducible receptor for mycobacterial cord factor, is the key switch for the transition of macrophages from cytokine expression to high nitric oxide production. In addition to its stimulatory role on TLR-mediated transcription, Mincle enhanced the translation of key genes required for nitric oxide synthesis through p38 and eIF5A hypusination, leading to granuloma resolution. Thus, Mincle has dual functions in the promotion and subsequent resolution of inflammation during anti-mycobacterial defence using both transcriptional and translational controls.
[Mh] Termos MeSH primário: Inflamação/genética
Lectinas Tipo C/genética
Proteínas de Membrana/genética
Óxido Nítrico/biossíntese
Biossíntese de Proteínas/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Células Cultivadas
Fatores Corda/metabolismo
Fatores Corda/farmacologia
Citocinas/metabolismo
Expressão Gênica/efeitos dos fármacos
Granuloma/genética
Granuloma/metabolismo
Immunoblotting
Inflamação/metabolismo
Lectinas Tipo C/metabolismo
Lisina/análogos & derivados
Lisina/metabolismo
Macrófagos/metabolismo
Proteínas de Membrana/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Mycobacterium tuberculosis/metabolismo
Células NIH 3T3
Óxido Nítrico Sintase Tipo II/genética
Óxido Nítrico Sintase Tipo II/metabolismo
Fatores de Iniciação de Peptídeos/genética
Fatores de Iniciação de Peptídeos/metabolismo
Proteínas de Ligação a RNA/genética
Proteínas de Ligação a RNA/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Receptores Toll-Like/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Clecsf8 protein, mouse); 0 (Cord Factors); 0 (Cytokines); 0 (Lectins, C-Type); 0 (Membrane Proteins); 0 (Peptide Initiation Factors); 0 (RNA-Binding Proteins); 0 (Toll-Like Receptors); 0 (eukaryotic translation initiation factor 5A); 31C4KY9ESH (Nitric Oxide); 3874VXF092 (hypusine); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160419
[St] Status:MEDLINE
[do] DOI:10.1038/ncomms11322


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[PMID]:26968340
[Au] Autor:Donnachie E; Fedotova EP; Hwang SA
[Ad] Endereço:Gulf States Hemophilia and Thrombophilia Center, Department of Pediatrics, University of Texas Medical School at Houston, Houston, Texas.
[Ti] Título:Trehalose 6,6-Dimycolate from Mycobacterium tuberculosis Induces Hypercoagulation.
[So] Source:Am J Pathol;186(5):1221-33, 2016 May.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tuberculosis (TB) remains a global health concern. Trehalose 6'6-dimycolate (TDM) activates innate inflammation and likely also stimulates chronic inflammation observed during disease progression. Noninfectious models using purified TDM oil/water emulsions elicit pathologic findings observed in patients with TB. We introduce a new TDM model that promotes inflammatory lung pathologic findings and vascular occlusion and hemorrhage. C57BL/6 and BALB/c mice were injected with 10 µg of i.p. TDM in light mineral oil (TDM-IP). At day 7, another injection of 10 µg of i.v. TDM in oil/water emulsion was given (TDM-IV). The i.p./i.v. TDM (TDM-IVIP) group was compared with mice injected once with i.v. or i.p. TDM. The responses to TDM-IP, TDM-IV, or TDM-IPIV were consistent between mouse strains. Mice that received TDM-IV and TDM-IPIV had inflammatory pathologic findings with increases in inflammatory and T-cell cytokines, and the TDM-IPIV group had further enhancement of IL-10 and granulocyte-macrophage colony-stimulating factor. The TDM-IPIV group had increased CD4(+) T cells in lung tissue, significantly increased coagulation, decreased clot formation time, and increased maximum clot firmness. Masson's trichrome staining revealed increased deposition of collagen in the occluded vasculature. TDM-IPIV promotes a hypercoagulopathy state, independent of inflammation. This new model argues that TDM is sufficient to generate the hypercoagulopathy observed in patients with TB.
[Mh] Termos MeSH primário: Adjuvantes Imunológicos/toxicidade
Fatores Corda/toxicidade
Trombofilia/induzido quimicamente
[Mh] Termos MeSH secundário: Animais
Antígenos CD/metabolismo
Colágeno/metabolismo
Citocinas/metabolismo
Modelos Animais de Doenças
Feminino
Fator Estimulador de Colônias de Granulócitos e Macrófagos/biossíntese
Imunidade Inata/efeitos dos fármacos
Pulmão/irrigação sanguínea
Pulmão/imunologia
Linfócitos/imunologia
Macrófagos/imunologia
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Mycobacterium tuberculosis
Neutrófilos/imunologia
Pneumonia/induzido quimicamente
Pneumonia/imunologia
Pneumonia/patologia
Pneumopatia Veno-Oclusiva/induzido quimicamente
Pneumopatia Veno-Oclusiva/imunologia
Pneumopatia Veno-Oclusiva/patologia
Tromboelastografia/métodos
Trombofilia/imunologia
Trombofilia/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Antigens, CD); 0 (Cord Factors); 0 (Cytokines); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor); 9007-34-5 (Collagen)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170522
[Lr] Data última revisão:
170522
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160313
[St] Status:MEDLINE


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[PMID]:26939595
[Au] Autor:Patin EC; Willcocks S; Orr S; Ward TH; Lang R; Schaible UE
[Ad] Endereço:Department of Immunology and Infection, Faculty of Infectious and Tropical Disease, London School of Hygiene and Tropical Medicine, London, UK Priority Area Infections, Research Center Borstel, Borstel, Germany Institute of Infection and Immunity, School of Medicine, Cardiff University, Cardiff, UK.
[Ti] Título:Mincle-mediated anti-inflammatory IL-10 response counter-regulates IL-12 in vitro.
[So] Source:Innate Immun;22(3):181-5, 2016 Apr.
[Is] ISSN:1753-4267
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The role of macrophage-inducible C-type lectin (Mincle) in anti-inflammatory responses has not yet been fully characterized. Herein, we show that engagement of Mincle by trehalose-dimycolate or mycobacteria promotes IL-10 production in macrophages, which causes down-regulation of IL-12p40 secretion. Thus, Mincle mediates both pro- as well as anti-inflammatory responses.
[Mh] Termos MeSH primário: Lectinas Tipo C/metabolismo
Macrófagos/imunologia
Proteínas de Membrana/metabolismo
Mycobacteriaceae/imunologia
Mycobacterium bovis/imunologia
Tuberculose Pulmonar/imunologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Fatores Corda/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Imunidade Inata
Interleucina-10/genética
Interleucina-10/metabolismo
Subunidade p40 da Interleucina-12/genética
Subunidade p40 da Interleucina-12/metabolismo
Lectinas Tipo C/genética
Macrófagos/microbiologia
Proteínas de Membrana/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptor 2 Toll-Like/genética
Receptor 2 Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Clecsf8 protein, mouse); 0 (Cord Factors); 0 (Interleukin-12 Subunit p40); 0 (Lectins, C-Type); 0 (Membrane Proteins); 0 (Tlr2 protein, mouse); 0 (Toll-Like Receptor 2); 130068-27-8 (Interleukin-10)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160305
[St] Status:MEDLINE
[do] DOI:10.1177/1753425916636671


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[PMID]:26625715
[Au] Autor:Singh N; Sreenivas V; Sheoran A; Sharma S; Gupta KB; Khuller GK; Mehta PK
[Ad] Endereço:Centre for Biotechnology, Maharshi Dayanand University (MDU), Rohtak 124001, Haryana, India.
[Ti] Título:Serodiagnostic potential of immuno-PCR using a cocktail of mycobacterial antigen 85B, ESAT-6 and cord factor in tuberculosis patients.
[So] Source:J Microbiol Methods;120:56-64, 2016 Jan.
[Is] ISSN:1872-8359
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:A novel indirect immuno-polymerase chain reaction (I-PCR) assay was developed for the detection of circulating anti-Ag85B (antigen 85B, Rv1886c), anti-ESAT-6 (early secretory antigenic target-6, Rv3875) and anti-cord factor (trehalose 6,6'-dimycolate) antibodies from the sera samples of pulmonary tuberculosis (PTB) and extrapulmonary tuberculosis (EPTB) patients and the results were compared with an analogous enzyme-linked immunosorbent assay (ELISA). We covalently attached the amino-modified reporter DNA to the dithiothreitol (DTT)-reduced anti-human IgG antibody through a chemical linker succinimidyl 4-[N-maleimidomethyl]-cyclohexane-1-carboxylate (SMCC). The detection of cocktail of anti-Ag85B, anti-ESAT-6 and anti-cord factor antibodies was found to be superior to the detection of individual antibodies. The sensitivities of 89.5% and 77.5% with I-PCR and 70.8% and 65% with ELISA were observed in smear-positive and smear-negative PTB cases, respectively with high specificity (90.9%). On the other hand, a sensitivity of 77.5% with I-PCR and 65% with ELISA was observed in EBTB cases. The detection of cocktail of antibodies by I-PCR is likely to improve the utility of existing algorithms for TB diagnosis.
[Mh] Termos MeSH primário: Aciltransferases/imunologia
Antígenos de Bactérias/imunologia
Proteínas de Bactérias/imunologia
Fatores Corda/imunologia
Mycobacterium tuberculosis/imunologia
Reação em Cadeia da Polimerase/métodos
Testes Sorológicos/métodos
Tuberculose/diagnóstico
[Mh] Termos MeSH secundário: Aciltransferases/sangue
Adolescente
Adulto
Anticorpos Antibacterianos/sangue
Anticorpos Antibacterianos/imunologia
Especificidade de Anticorpos
Antígenos de Bactérias/sangue
Proteínas de Bactérias/sangue
Fatores Corda/sangue
Ditiotreitol/química
Ditiotreitol/imunologia
Ensaio de Imunoadsorção Enzimática/métodos
Seres Humanos
Imunoensaio/métodos
Imunoglobulina G/sangue
Imunoglobulina G/química
Maleimidas
Meia-Idade
Tuberculose/sangue
Tuberculose/imunologia
Tuberculose Pulmonar/sangue
Tuberculose Pulmonar/diagnóstico
Tuberculose Pulmonar/imunologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Bacterial); 0 (Antigens, Bacterial); 0 (Bacterial Proteins); 0 (Cord Factors); 0 (ESAT-6 protein, Mycobacterium tuberculosis); 0 (Immunoglobulin G); 0 (Maleimides); 64987-85-5 (N-(4-carboxycyclohexylmethyl)maleimide N-hydroxysuccinimide ester); EC 2.3.- (Acyltransferases); EC 2.3.1.- (antigen 85C, Mycobacterium tuberculosis); T8ID5YZU6Y (Dithiothreitol)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151203
[St] Status:MEDLINE


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[PMID]:26558717
[Au] Autor:Kerscher B; Wilson GJ; Reid DM; Mori D; Taylor JA; Besra GS; Yamasaki S; Willment JA; Brown GD
[Ad] Endereço:Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, UK.
[Ti] Título:Mycobacterial receptor, Clec4d (CLECSF8, MCL), is coregulated with Mincle and upregulated on mouse myeloid cells following microbial challenge.
[So] Source:Eur J Immunol;46(2):381-9, 2016 Feb.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The C-type lectin receptor (CTLR), Clec4d (MCL, CLECSF8), is a member of the Dectin-2 cluster of CTLRs, which also includes the related receptors Mincle and Dectin-2. Like Mincle, Clec4d recognizes mycobacterial cord factor, trehalose dimycolate, and we recently demonstrated its key role in anti-mycobacterial immunity in mouse and man. Here, we characterized receptor expression in naïve mice, under inflammatory conditions, and during Mycobacterium bovis BCG infection using newly generated monoclonal antibodies. In naïve mice, Clec4d was predominantly expressed on myeloid cells within the peritoneal cavity, blood, and bone marrow. Unexpectedly, basal expression of Clec4d was very low on leukocytes in the lung. However, receptor expression was significantly upregulated on pulmonary myeloid cells during M. bovis BCG infection. Moreover, Clec4d expression could be strongly induced in vitro and in vivo by various microbial stimuli, including TLR agonists, but not exogenous cytokines. Notably, we show that Clec4d requires association with the signaling adaptor FcRγ and Mincle, but not Dectin-2, for surface expression. In addition, we provide evidence that Clec4d and Mincle, but not Dectin-2, are interdependently coregulated during inflammation and infection. These data show that Clec4d is an inducible myeloid-expressed CTLR in mice, whose expression is tightly linked to that of Mincle.
[Mh] Termos MeSH primário: Fatores Corda/metabolismo
Lectinas Tipo C/metabolismo
Leucócitos/imunologia
Mycobacterium bovis/imunologia
Células Mieloides/imunologia
Receptores de IgG/metabolismo
Receptores Imunológicos/metabolismo
Tuberculose/imunologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Regulação da Expressão Gênica
Interações Hospedeiro-Patógeno
Imunidade Inata
Lectinas Tipo C/genética
Leucócitos/microbiologia
Pulmão/microbiologia
Pulmão/patologia
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Mycobacterium bovis/metabolismo
Células Mieloides/microbiologia
Cavidade Peritoneal/microbiologia
Cavidade Peritoneal/patologia
Receptores Imunológicos/genética
Transdução de Sinais
Tuberculose/veterinária
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Clec4d protein, mouse); 0 (Clecsf8 protein, mouse); 0 (Cord Factors); 0 (Lectins, C-Type); 0 (Membrane Proteins); 0 (Receptors, IgG); 0 (Receptors, Immunologic); 0 (dectin-2, mouse)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151113
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201545858



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