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Pesquisa : B03.510.024.049.525.500.720.500 [Categoria DeCS]
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[PMID]:29281637
[Au] Autor:Boot M; van Winden VJC; Sparrius M; van de Weerd R; Speer A; Ummels R; Rustad T; Sherman DR; Bitter W
[Ad] Endereço:Department of Medical Microbiology and Infection Control, VU University Medical Center, Amsterdam, the Netherlands.
[Ti] Título:Cell envelope stress in mycobacteria is regulated by the novel signal transduction ATPase IniR in response to trehalose.
[So] Source:PLoS Genet;13(12):e1007131, 2017 12.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cell envelope of mycobacteria is a highly unique and complex structure that is functionally equivalent to that of Gram-negative bacteria to protect the bacterial cell. Defects in the integrity or assembly of this cell envelope must be sensed to allow the induction of stress response systems. The promoter that is specifically and most strongly induced upon exposure to ethambutol and isoniazid, first line drugs that affect cell envelope biogenesis, is the iniBAC promoter. In this study, we set out to identify the regulator of the iniBAC operon in Mycobacterium marinum using an unbiased transposon mutagenesis screen in a constitutively iniBAC-expressing mutant background. We obtained multiple mutants in the mce1 locus as well as mutants in an uncharacterized putative transcriptional regulator (MMAR_0612). This latter gene was shown to function as the iniBAC regulator, as overexpression resulted in constitutive iniBAC induction, whereas a knockout mutant was unable to respond to the presence of ethambutol and isoniazid. Experiments with the M. tuberculosis homologue (Rv0339c) showed identical results. RNAseq experiments showed that this regulatory gene was exclusively involved in the regulation of the iniBAC operon. We therefore propose to name this dedicated regulator iniBAC Regulator (IniR). IniR belongs to the family of signal transduction ATPases with numerous domains, including a putative sugar-binding domain. Upon testing different sugars, we identified trehalose as an activator and metabolic cue for iniBAC activation, which could also explain the effect of the mce1 mutations. In conclusion, cell envelope stress in mycobacteria is regulated by IniR in a cascade that includes trehalose.
[Mh] Termos MeSH primário: Adenosina Trifosfatases/genética
Mycobacterium marinum/genética
Mycobacterium marinum/metabolismo
Trealose/metabolismo
[Mh] Termos MeSH secundário: Proteínas de Bactérias/genética
Membrana Celular/metabolismo
Parede Celular/genética
Parede Celular/metabolismo
Elementos de DNA Transponíveis
Regulação Bacteriana da Expressão Gênica
Genes Bacterianos
Mutagênese Insercional
Óperon
Regiões Promotoras Genéticas
Transdução de Sinais
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (DNA Transposable Elements); B8WCK70T7I (Trehalose); EC 3.6.1.- (Adenosine Triphosphatases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171228
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007131


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[PMID]:28873466
[Au] Autor:Dharra R; Talwar S; Singh Y; Gupta R; Cirillo JD; Pandey AK; Kulharia M; Mehta PK
[Ad] Endereço:Centre for Biotechnology, Maharshi Dayanand University (MDU), Rohtak, India.
[Ti] Título:Rational design of drug-like compounds targeting Mycobacterium marinum MelF protein.
[So] Source:PLoS One;12(9):e0183060, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mycobacterial mel2 locus (mycobacterial enhanced infection locus, Rv1936-1941) is Mycobacterium marinum and M. tuberculosis specific, which can withstand reactive oxygen species (ROS) and reactive nitrogen species (RNS) induced stress. A library of over a million compounds was screened using in silico virtual ligand screening (VLS) to identify inhibitors against the modeled structure of MelF protein expressed by melF of mel2 locus so that M. marinum's ability to withstand ROS/RNS stress could be reduced. The top ranked 1000 compounds were further screened to identify 178 compounds to maximize the scaffold diversity by manually evaluating the interaction of each compound with the target site. M. marinum melF was cloned, expressed and purified as maltose binding protein (MBP)-tagged recombinant protein in Escherichia coli. After establishing the flavin dependent oxidoreductase activity of MelF (~ 84 kDa), the inhibitors were screened for the inhibition of enzyme activity of whole cell lysate (WCL) and the purified MelF. Amongst these, 16 compounds could significantly inhibit the enzyme activity of purified MelF. For the six best inhibitory compounds, the minimal inhibitory concentration (MIC) was determined to be 3.4-19.4 µM and 13.5-38.8 µM for M. marinum and M. tuberculosis, respectively. Similarly, the minimal bactericidal concentration (MBC) was determined to be 6.8-38.8 µM and 27-38.8 µM against M. marinum and M. tuberculosis, respectively. One compound each in combination with isoniazid (INH) also showed synergistic inhibitory effect against M. marinum and M. tuberculosis with no cytotoxicity in HeLa cells. Interestingly, these inhibitors did not display any non-specific protein-structure destabilizing effect. Such inhibitors targeting the anti-ROS/RNS machinery may facilitate the efficient killing of replicating and nonreplicating mycobacteria inside the host cells.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Proteínas de Bactérias/metabolismo
Desenho de Drogas
Mycobacterium marinum/efeitos dos fármacos
[Mh] Termos MeSH secundário: Proteínas de Bactérias/química
Proteínas de Bactérias/isolamento & purificação
Cromatografia Líquida de Alta Pressão
Dicroísmo Circular
Clonagem Molecular
Contagem de Colônia Microbiana
Avaliação Pré-Clínica de Medicamentos
Inibidores Enzimáticos/análise
Inibidores Enzimáticos/química
Inibidores Enzimáticos/farmacologia
Flavinas/metabolismo
Cinética
Modelos Lineares
Testes de Sensibilidade Microbiana
Simulação de Acoplamento Molecular
Mycobacterium marinum/crescimento & desenvolvimento
Mycobacterium tuberculosis/efeitos dos fármacos
Mycobacterium tuberculosis/crescimento & desenvolvimento
Estrutura Secundária de Proteína
Homologia Estrutural de Proteína
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Bacterial Proteins); 0 (Enzyme Inhibitors); 0 (Flavins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170906
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183060


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[PMID]:28841420
[Au] Autor:Madigan CA; Cambier CJ; Kelly-Scumpia KM; Scumpia PO; Cheng TY; Zailaa J; Bloom BR; Moody DB; Smale ST; Sagasti A; Modlin RL; Ramakrishnan L
[Ad] Endereço:Division of Dermatology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Department of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA
[Ti] Título:A Macrophage Response to Mycobacterium leprae Phenolic Glycolipid Initiates Nerve Damage in Leprosy.
[So] Source:Cell;170(5):973-985.e10, 2017 Aug 24.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mycobacterium leprae causes leprosy and is unique among mycobacterial diseases in producing peripheral neuropathy. This debilitating morbidity is attributed to axon demyelination resulting from direct interaction of the M. leprae-specific phenolic glycolipid 1 (PGL-1) with myelinating glia and their subsequent infection. Here, we use transparent zebrafish larvae to visualize the earliest events of M. leprae-induced nerve damage. We find that demyelination and axonal damage are not directly initiated by M. leprae but by infected macrophages that patrol axons; demyelination occurs in areas of intimate contact. PGL-1 confers this neurotoxic response on macrophages: macrophages infected with M. marinum-expressing PGL-1 also damage axons. PGL-1 induces nitric oxide synthase in infected macrophages, and the resultant increase in reactive nitrogen species damages axons by injuring their mitochondria and inducing demyelination. Our findings implicate the response of innate macrophages to M. leprae PGL-1 in initiating nerve damage in leprosy.
[Mh] Termos MeSH primário: Antígenos de Bactérias/metabolismo
Modelos Animais de Doenças
Glicolipídeos/metabolismo
Hanseníase/microbiologia
Hanseníase/patologia
Macrófagos/imunologia
Mycobacterium leprae/fisiologia
[Mh] Termos MeSH secundário: Animais
Axônios/metabolismo
Axônios/patologia
Doenças Desmielinizantes
Larva/crescimento & desenvolvimento
Hanseníase/imunologia
Mycobacterium marinum/metabolismo
Bainha de Mielina/química
Bainha de Mielina/metabolismo
Bainha de Mielina/ultraestrutura
Neuroglia/metabolismo
Neuroglia/patologia
Óxido Nítrico/metabolismo
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Bacterial); 0 (Glycolipids); 0 (phenolic glycolipid I, Mycobacterium leprae); 31C4KY9ESH (Nitric Oxide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170826
[St] Status:MEDLINE


  4 / 585 MEDLINE  
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[PMID]:28727774
[Au] Autor:Ouertatani-Sakouhi H; Kicka S; Chiriano G; Harrison CF; Hilbi H; Scapozza L; Soldati T; Cosson P
[Ad] Endereço:Faculty of Medicine, Department of Cell Physiology and Metabolism, University of Geneva, Geneva, Switzerland.
[Ti] Título:Inhibitors of Mycobacterium marinum virulence identified in a Dictyostelium discoideum host model.
[So] Source:PLoS One;12(7):e0181121, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tuberculosis remains one of the major threats to public health worldwide. Given the prevalence of multi drug resistance (MDR) in Mycobacterium tuberculosis strains, there is a strong need to develop new anti-mycobacterial drugs with modes of action distinct from classical antibiotics. Inhibitors of mycobacterial virulence might target new molecular processes and may represent a potential new therapeutic alternative. In this study, we used a Dictyostelium discoideum host model to assess virulence of Mycobacterium marinum and to identify compounds inhibiting mycobacterial virulence. Among 9995 chemical compounds, we selected 12 inhibitors of mycobacterial virulence that do not inhibit mycobacterial growth in synthetic medium. Further analyses revealed that 8 of them perturbed functions requiring an intact mycobacterial cell wall such as sliding motility, bacterial aggregation or cell wall permeability. Chemical analogs of two compounds were analyzed. Chemical modifications altered concomitantly their effect on sliding motility and on mycobacterial virulence, suggesting that the alteration of the mycobacterial cell wall caused the loss of virulence. We characterized further one of the selected compounds and found that it inhibited the ability of mycobacteria to replicate in infected cells. Together these results identify new antimycobacterial compounds that represent new tools to unravel the molecular mechanisms controlling mycobacterial pathogenicity. The isolation of compounds with anti-virulence activity is the first step towards developing new antibacterial treatments.
[Mh] Termos MeSH primário: Dictyostelium/microbiologia
Mycobacterium marinum/efeitos dos fármacos
Virulência/efeitos dos fármacos
[Mh] Termos MeSH secundário: Avaliação Pré-Clínica de Medicamentos/métodos
Mycobacterium marinum/patogenicidade
Mycobacterium marinum/fisiologia
Mycobacterium marinum/ultraestrutura
Bibliotecas de Moléculas Pequenas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Small Molecule Libraries)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181121


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[PMID]:28629484
[Au] Autor:Yacisin K; Hsieh JL; Weiss D; Ackelsberg J; Lee E; Jones L; Leung YL; Li L; Yung J; Slavinski S; Hanson H; Ridpath A; Kornblum J; Lin Y; Robbe-Austerman S; Rakeman J; Siemetzki-Kapoor U; Stuber T; Greene SK
[Ad] Endereço:Division of Disease Control,New York City Department of Health and Mental Hygiene,Queens, New York,USA.
[Ti] Título:Outbreak of non-tuberculous mycobacteria skin or soft tissue infections associated with handling fish - New York City, 2013-2014.
[So] Source:Epidemiol Infect;145(11):2269-2279, 2017 08.
[Is] ISSN:1469-4409
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mycobacterium marinum, a bacterium found in freshwater and saltwater, can infect persons with direct exposure to fish or aquariums. During December 2013, the New York City Department of Health and Mental Hygiene learned of four suspected or confirmed M. marinum skin or soft tissue infections (SSTIs) among persons who purchased whole fish from Chinese markets. Ninety-eight case-patients with non-tuberculous mycobacteria (NTM) SSTIs were identified with onset June 2013-March 2014. Of these, 77 (79%) were female. The median age was 62 years (range 30-91). Whole genome sequencing of clinical isolates revealed two main clusters and marked genetic diversity. Environmental samples from distributors yielded NTM though not M. marinum. We compared 56 case-patients with 185 control subjects who shopped in Chinese markets, frequency-matched by age group and sex. Risk factors for infection included skin injury to the finger or hand (odds ratio [OR]: 15·5; 95% confidence interval [CI]: 6·9-37·3), hand injury while preparing fish or seafood (OR 8·3; 95% CI 3·8-19·1), and purchasing tilapia (OR 3·6; 95% CI 1·1-13·9) or whiting (OR 2·7; 95% CI 1·1-6·6). A definitive environmental outbreak source was not identified.
[Mh] Termos MeSH primário: Surtos de Doenças
Infecções por Micobactéria não Tuberculosa/epidemiologia
Mycobacterium marinum/isolamento & purificação
Dermatopatias Bacterianas/epidemiologia
Infecções dos Tecidos Moles/epidemiologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Estudos de Casos e Controles
Feminino
Peixes
Seres Humanos
Incidência
Masculino
Meia-Idade
Infecções por Micobactéria não Tuberculosa/microbiologia
Cidade de Nova Iorque/epidemiologia
Dermatopatias Bacterianas/microbiologia
Infecções dos Tecidos Moles/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE
[do] DOI:10.1017/S0950268817001066


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[PMID]:28549155
[Au] Autor:Prasai K; Robinson LC; Scott RS; Tatchell K; Harrison L
[Ad] Endereço:Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA.
[Ti] Título:Evidence for double-strand break mediated mitochondrial DNA replication in Saccharomyces cerevisiae.
[So] Source:Nucleic Acids Res;45(13):7760-7773, 2017 Jul 27.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The mechanism of mitochondrial DNA (mtDNA) replication in Saccharomyces cerevisiae is controversial. Evidence exists for double-strand break (DSB) mediated recombination-dependent replication at mitochondrial replication origin ori5 in hypersuppressive ρ- cells. However, it is not clear if this replication mode operates in ρ+ cells. To understand this, we targeted bacterial Ku (bKu), a DSB binding protein, to the mitochondria of ρ+ cells with the hypothesis that bKu would bind persistently to mtDNA DSBs, thereby preventing mtDNA replication or repair. Here, we show that mitochondrial-targeted bKu binds to ori5 and that inducible expression of bKu triggers petite formation preferentially in daughter cells. bKu expression also induces mtDNA depletion that eventually results in the formation of ρ0 cells. This data supports the idea that yeast mtDNA replication is initiated by a DSB and bKu inhibits mtDNA replication by binding to a DSB at ori5, preventing mtDNA segregation to daughter cells. Interestingly, we find that mitochondrial-targeted bKu does not decrease mtDNA content in human MCF7 cells. This finding is in agreement with the fact that human mtDNA replication, typically, is not initiated by a DSB. Therefore, this study provides evidence that DSB-mediated replication is the predominant form of mtDNA replication in ρ+ yeast cells.
[Mh] Termos MeSH primário: Quebras de DNA de Cadeia Dupla
Replicação do DNA
DNA Fúngico/metabolismo
DNA Mitocondrial/metabolismo
Saccharomyces cerevisiae/metabolismo
[Mh] Termos MeSH secundário: Proteínas de Bactérias/genética
Proteínas de Bactérias/metabolismo
Replicação do DNA/genética
DNA Fúngico/genética
DNA Mitocondrial/genética
DNA Liase (Sítios Apurínicos ou Apirimidínicos)/genética
DNA Liase (Sítios Apurínicos ou Apirimidínicos)/metabolismo
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Genes Fúngicos
Seres Humanos
Células MCF-7
Modelos Biológicos
Mutação
Mycobacterium marinum/genética
Mycobacterium marinum/metabolismo
Origem de Replicação
Saccharomyces cerevisiae/genética
Proteínas de Saccharomyces cerevisiae/genética
Proteínas de Saccharomyces cerevisiae/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (DNA, Fungal); 0 (DNA, Mitochondrial); 0 (DNA-Binding Proteins); 0 (Saccharomyces cerevisiae Proteins); EC 4.2.99.18 (DNA-(Apurinic or Apyrimidinic Site) Lyase); EC 4.2.99.18 (NTG1 protein, S cerevisiae)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx443


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[PMID]:28414774
[Au] Autor:Cardenal-Muñoz E; Arafah S; López-Jiménez AT; Kicka S; Falaise A; Bach F; Schaad O; King JS; Hagedorn M; Soldati T
[Ad] Endereço:Department of Biochemistry, Faculty of Sciences, Sciences II, University of Geneva, Geneva, Switzerland.
[Ti] Título:Mycobacterium marinum antagonistically induces an autophagic response while repressing the autophagic flux in a TORC1- and ESX-1-dependent manner.
[So] Source:PLoS Pathog;13(4):e1006344, 2017 Apr.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Autophagy is a eukaryotic catabolic process also participating in cell-autonomous defence. Infected host cells generate double-membrane autophagosomes that mature in autolysosomes to engulf, kill and digest cytoplasmic pathogens. However, several bacteria subvert autophagy and benefit from its machinery and functions. Monitoring infection stages by genetics, pharmacology and microscopy, we demonstrate that the ESX-1 secretion system of Mycobacterium marinum, a close relative to M. tuberculosis, upregulates the transcription of autophagy genes, and stimulates autophagosome formation and recruitment to the mycobacteria-containing vacuole (MCV) in the host model organism Dictyostelium. Antagonistically, ESX-1 is also essential to block the autophagic flux and deplete the MCV of proteolytic activity. Activators of the TORC1 complex localize to the MCV in an ESX-1-dependent manner, suggesting an important role in the manipulation of autophagy by mycobacteria. Our findings suggest that the infection by M. marinum activates an autophagic response that is simultaneously repressed and exploited by the bacterium to support its survival inside the MCV.
[Mh] Termos MeSH primário: Autofagia
Proteínas de Bactérias/metabolismo
Complexos Multiproteicos/metabolismo
Infecções por Micobactéria não Tuberculosa/metabolismo
Infecções por Micobactéria não Tuberculosa/fisiopatologia
Mycobacterium marinum/metabolismo
Serina-Treonina Quinases TOR/metabolismo
[Mh] Termos MeSH secundário: Proteínas de Bactérias/genética
Dictyostelium/genética
Dictyostelium/metabolismo
Dictyostelium/microbiologia
Interações Hospedeiro-Patógeno
Seres Humanos
Alvo Mecanístico do Complexo 1 de Rapamicina
Complexos Multiproteicos/genética
Infecções por Micobactéria não Tuberculosa/genética
Infecções por Micobactéria não Tuberculosa/virologia
Mycobacterium marinum/genética
Serina-Treonina Quinases TOR/genética
Vacúolos/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Multiprotein Complexes); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006344


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[PMID]:28387180
[Au] Autor:Aubry A; Mougari F; Reibel F; Cambau E
[Ad] Endereço:Centre National de Référence des mycobactéries et résistance des Mycobactéries aux antituberculeux.
[Ti] Título:Mycobacterium marinum.
[So] Source:Microbiol Spectr;5(2), 2017 Apr.
[Is] ISSN:2165-0497
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mycobacterium marinum is a well-known pathogenic mycobacterium for skin and soft tissue infections and is associated with fishes and water. Among nontuberculous mycobacteria (NTM), it is the leading cause of extrarespiratory human infections worldwide. In addition, there is a specific scientific interest in M. marinum because of its genetic relatedness to Mycobacterium tuberculosis and because experimental infection of M. marinum in fishes mimics tuberculosis pathogenesis. Microbiological characteristics include the fact that it grows in 7 to 14 days with photochromogenic colonies and is difficult to differentiate from Mycobacterium ulcerans and other mycolactone-producing NTM on a molecular basis. The diagnosis is highly suspected by the mode of infection, which is related to the hobby of fishkeeping, professional handling of marine shells, or swimming in nonchlorinated pools. Clinics distinguished skin and soft tissue lesions (typically sporotrichoid or subacute hand nodules) and lesions disseminated to joint and bone, often related with the local use of corticosteroids. In clinical microbiology, microscopy and culture are often negative because growth requires low temperature (30°C) and several weeks to succeed in primary cultivation. The treatment is not standardized, and no randomized control trials have been done. Therapy is a combination of surgery and antimicrobial agents such as cyclines and rifampin, with successful outcome in most of the skin diseases but less frequently in deep tissue infections. Prevention can be useful with hand protection recommendations for professionals and all persons manipulating fishes or fish tank water and use of alcohol disinfection after contact.
[Mh] Termos MeSH primário: Infecções por Micobactéria não Tuberculosa/microbiologia
Mycobacterium marinum/fisiologia
[Mh] Termos MeSH secundário: Animais
Suscetibilidade a Doenças
Ecossistema
Doenças dos Peixes/tratamento farmacológico
Doenças dos Peixes/microbiologia
Doenças dos Peixes/prevenção & controle
Peixes/microbiologia
Seres Humanos
Infecções por Micobactéria não Tuberculosa/diagnóstico
Infecções por Micobactéria não Tuberculosa/prevenção & controle
Infecções por Micobactéria não Tuberculosa/veterinária
Dermatopatias Bacterianas/diagnóstico
Dermatopatias Bacterianas/tratamento farmacológico
Dermatopatias Bacterianas/microbiologia
Dermatopatias Bacterianas/cirurgia
Microbiologia da Água
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170627
[Lr] Data última revisão:
170627
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170408
[St] Status:MEDLINE
[do] DOI:10.1128/microbiolspec.TNMI7-0038-2016


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[PMID]:28322210
[Au] Autor:Li WT; Chang HW; Pang VF; Wang FI; Liu CH; Chen TY; Guo JC; Wada T; Jeng CR
[Ad] Endereço:Graduate Institute of Molecular and Comparative Pathobiology, School of Veterinary Medicine, National Taiwan University, No. 1, Sec. 4, Roosevelt Rd, Taipei 10617, Taiwan.
[Ti] Título:Mycolactone-producing Mycobacterium marinum infection in captive Hong Kong warty newts and pathological evidence of impaired host immune function.
[So] Source:Dis Aquat Organ;123(3):239-249, 2017 Mar 21.
[Is] ISSN:0177-5103
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:A mass mortality event of captive Hong Kong warty newts Paramesotriton hongkongensis with non-granulomatous necrotic lesions occurred in Taipei Zoo, Taiwan, in 2014. Clinically, the sick newts were lethargic and often covered with water mold Saprolegnia sp. on the skin of the body trunk or extremities. Predominant pathological findings were multifocal non-granulomatous necrotic lesions in the liver, spleen, and kidneys and severe skin infection with Saprolegnia sp., with deep invasion and involvement of underlying muscles. The possibility of ranavirus infection was ruled out by negative PCR results. Unexpectedly, abundant intralesional acid-fast positive bacilli were found in the necrotic lesions of the liver, spleen, and kidney in all 14 sick newts. PCR targeting the hsp65, ITS region, and partial 16S rRNA genes was performed, and the sequence identity from amplified amplicons of hsp65 and partial 16S rRNA genes was 100% identical to that of the corresponding gene fragment of Mycobacterium marinum. Further molecular investigations demonstrated that the current M. marinum was a mycolactone-producing mycobacterium with the presence of esxA/esxB genes. Mycolactone is a plasmid-encoded, immunosuppressive, and cytotoxic toxin. The possible immunosuppression phenomenon characterized by systemic non-granulomatous necrotic lesions caused by M. marinum and the unusual deep invasive infection caused by water mold might be associated with the immunosuppressive effect of mycolactone. Therefore, it should be noted that non-granulomatous necrotic lesions in amphibians can be caused not only by ranavirus infection but also by mycobacteriosis.
[Mh] Termos MeSH primário: Macrolídeos/metabolismo
Infecções por Micobactéria não Tuberculosa/veterinária
Mycobacterium marinum/metabolismo
Salamandridae/microbiologia
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
DNA Bacteriano/genética
Infecções por Micobactéria não Tuberculosa/imunologia
Infecções por Micobactéria não Tuberculosa/microbiologia
Infecções por Micobactéria não Tuberculosa/mortalidade
Mycobacterium marinum/genética
Salamandridae/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Bacterial); 0 (Macrolides); 0 (mycolactone)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE
[do] DOI:10.3354/dao03092


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[PMID]:28298234
[Au] Autor:Teixeira PG; Ferreira R; Zhou YJ; Siewers V; Nielsen J
[Ad] Endereço:Department of Biology and Biological Engineering, Chalmers University of Technology, 412 96, Gothenburg, Sweden.
[Ti] Título:Dynamic regulation of fatty acid pools for improved production of fatty alcohols in Saccharomyces cerevisiae.
[So] Source:Microb Cell Fact;16(1):45, 2017 Mar 15.
[Is] ISSN:1475-2859
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In vivo production of fatty acid-derived chemicals in Saccharomyces cerevisiae requires strategies to increase the intracellular supply of either acyl-CoA or free fatty acids (FFAs), since their cytosolic concentrations are quite low in a natural state for this organism. Deletion of the fatty acyl-CoA synthetase genes FAA1 and FAA4 is an effective and straightforward way to disable re-activation of fatty acids and drastically increase FFA levels. However, this strategy causes FFA over-accumulation and consequential release to the extracellular medium, which results in a significant loss of precursors that compromises the process yield. In the present study, we aimed for dynamic expression of the fatty acyl-CoA synthetase gene FAA1 to regulate FFA and acyl-CoA pools in order to improve fatty alcohol production yields. RESULTS: We analyzed the metabolite dynamics of a faa1Δ faa4Δ strain constitutively expressing a carboxylic acid reductase from Mycobacterium marinum (MmCAR) and an endogenous alcohol dehydrogenase (Adh5) for in vivo production of fatty alcohols from FFAs. We observed production of fatty acids and fatty alcohols with different rates leading to high levels of FFAs not being converted to the final product. To address the issue, we expressed the MmCAR + Adh5 pathway together with a fatty acyl-CoA reductase from Marinobacter aquaeolei to enable fatty alcohol production simultaneously from FFA and acyl-CoA, respectively. Then, we expressed FAA1 under the control of different promoters in order to balance FFA and acyl-CoA interconversion rates and to achieve optimal levels for conversion to fatty alcohols. Expressing FAA1 under control of the HXT1 promoter led to an increased accumulation of fatty alcohols per OD up to 41% while FFA levels were decreased by 63% compared with the control strain. CONCLUSIONS: Fine-tuning and dynamic regulation of key metabolic steps can be used to improve cell factories when the rates of downstream reactions are limiting. This avoids loss of precursors to the extracellular medium or to competing reactions, hereby potentially improving the process yield. The study also provides knowledge of a key point of fatty acid regulation and homeostasis, which can be used for future design of cells factories for fatty acid-derived chemicals.
[Mh] Termos MeSH primário: Ácidos Graxos não Esterificados/metabolismo
Álcoois Graxos/metabolismo
Regulação Fúngica da Expressão Gênica
Saccharomyces cerevisiae/genética
Saccharomyces cerevisiae/metabolismo
[Mh] Termos MeSH secundário: Álcool Desidrogenase/genética
Coenzima A Ligases/genética
Marinobacter/genética
Engenharia Metabólica/métodos
Mycobacterium marinum/genética
Oxirredutases/genética
Regiões Promotoras Genéticas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids, Nonesterified); 0 (Fatty Alcohols); EC 1.- (Oxidoreductases); EC 1.1.1.1 (Alcohol Dehydrogenase); EC 1.3.99.- (carboxylic acid reductase); EC 6.2.1.- (Coenzyme A Ligases); EC 6.2.1.- (Faa1 protein, S cerevisiae)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170420
[Lr] Data última revisão:
170420
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170317
[St] Status:MEDLINE
[do] DOI:10.1186/s12934-017-0663-3



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