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[PMID]:29178652
[Au] Autor:Modi BP; Teves ME; Pearson LN; Parikh HI; Haymond-Thornburg H; Tucker JL; Chaemsaithong P; Gomez-Lopez N; York TP; Romero R; Strauss JF
[Ad] Endereço:Department of Human and Molecular Genetics, Virginia Commonwealth University, Richmond, Virginia.
[Ti] Título:Mutations in fetal genes involved in innate immunity and host defense against microbes increase risk of preterm premature rupture of membranes (PPROM).
[So] Source:Mol Genet Genomic Med;5(6):720-729, 2017 11.
[Is] ISSN:2324-9269
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Twin studies have revealed a significant contribution of the fetal genome to risk of preterm birth. Preterm premature rupture of membranes (PPROM) is the leading identifiable cause of preterm delivery. Infection and inflammation of the fetal membranes is commonly found associated with PPROM. METHODS: We carried out whole exome sequencing (WES) of genomic DNA from neonates born of African-American mothers whose pregnancies were complicated by PPROM (76) or were normal term pregnancies (N = 43) to identify mutations in 35 candidate genes involved in innate immunity and host defenses against microbes. Targeted genotyping of mutations in the candidates discovered by WES was conducted on an additional 188 PPROM cases and 175 controls. RESULTS: We identified rare heterozygous nonsense and frameshift mutations in several of the candidate genes, including CARD6, CARD8, DEFB1, FUT2, MBL2, NLP10, NLRP12, and NOD2. We discovered that some mutations (CARD6, DEFB1, FUT2, MBL2, NLRP10, NOD2) were present only in PPROM cases. CONCLUSIONS: We conclude that rare damaging mutations in innate immunity and host defense genes, the majority being heterozygous, are more frequent in neonates born of pregnancies complicated by PPROM. These findings suggest that the risk of preterm birth in African-Americans may be conferred by mutations in multiple genes encoding proteins involved in dampening the innate immune response or protecting the host against microbial infection and microbial products.
[Mh] Termos MeSH primário: Ruptura Prematura de Membranas Fetais/diagnóstico
Imunidade Inata/genética
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Sinalização CARD/genética
Estudos de Casos e Controles
Códon sem Sentido
DNA/química
DNA/isolamento & purificação
DNA/metabolismo
Feminino
Ruptura Prematura de Membranas Fetais/etiologia
Ruptura Prematura de Membranas Fetais/genética
Mutação da Fase de Leitura
Fucosiltransferases/genética
Seres Humanos
Recém-Nascido
Gravidez
Risco
Análise de Sequência de DNA
Sequenciamento Completo do Exoma
beta-Defensinas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Nm] Nome de substância:
0 (CARD Signaling Adaptor Proteins); 0 (CARD6 protein, human); 0 (Codon, Nonsense); 0 (DEFB1 protein, human); 0 (beta-Defensins); 9007-49-2 (DNA); EC 2.4.1.- (Fucosyltransferases); EC 2.4.1.69 (galactoside 2-alpha-L-fucosyltransferase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1002/mgg3.330


  2 / 2165 MEDLINE  
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[PMID]:28970736
[Au] Autor:Kazakos EI; Dorrell N; Polyzos SA; Deretzi G; Kountouras J
[Ad] Endereço:Department of Medicine, the Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, 54642 Thessaloniki, Greece. ekazakos@gmail.com.
[Ti] Título:Comment on "Effect of biofilm formation by clinical isolates of Helicobacter pylori on the efflux-mediated resistance to commonly used antibiotics".
[So] Source:World J Gastroenterol;23(33):6194-6196, 2017 Sep 07.
[Is] ISSN:2219-2840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Attaran et al have recently shown that decreased susceptibility of established biofilms to specific antibiotics, was associated with the overtly enhanced transcription of two efflux pump genes, and , involved in specific resistance to tetracycline and multiple antibiotics, respectively. Apart from antibiotic exposure, secretion of multiple antimicrobial peptides, such as human ß-defensins (hßDs), by the gastric epithelium upon challenge, may act as early triggering events that positively impact biofilm formation and thus, antibiotic resistance. In this regard, we undertook genomic transcriptional studies using 26695 strain following exposure to sublethal, similar to those present in the gastric niche, concentrations of hßDs in an attempt to provide preliminary data regarding possible mechanisms of immune evasion and selective sensitivity of . Our preliminary results indicate that hßD exposure ignites a rapid response that is largely due to the activation of several, possibly interconnected transcriptional regulatory networks - origons - that ultimately coordinate cellular processes needed to maintain homeostasis and successful adaptation of the bacterium in the gastric environment. In addition, we have shown that both antibiotic and hßD resistance are mediated by dedicated periplasmic transporters, including the aforementioned efflux pump genes and , involved in active export of antibiotics from the cell membrane and/or, as recently suggested, substrate sensing and signalling. Furthermore, it appears that sublethal doses of hßDs may enhance biofilm formation by the sustained expression of, mainly, quorum sensing-related genes. In conclusion, we provide additional data regarding the role of specific innate immune molecules in antibiotic cross-resistance mechanisms that may deepen our understanding in the context of the development of novel eradication regimens.
[Mh] Termos MeSH primário: Antibacterianos
Helicobacter pylori/efeitos dos fármacos
[Mh] Termos MeSH secundário: Biofilmes/efeitos dos fármacos
Resistência Microbiana a Medicamentos/efeitos dos fármacos
Seres Humanos
beta-Defensinas
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (beta-Defensins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.3748/wjg.v23.i33.6194


  3 / 2165 MEDLINE  
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[PMID]:28910369
[Au] Autor:Kumar NP; Moideen K; Viswanathan V; Sivakumar S; Menon PA; Kornfeld H; Babu S
[Ad] Endereço:National Institutes of Health-NIRT-International Center for Excellence in Research, Chennai, India.
[Ti] Título:Heightened circulating levels of antimicrobial peptides in tuberculosis-Diabetes co-morbidity and reversal upon treatment.
[So] Source:PLoS One;12(9):e0184753, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The association of antimicrobial peptides (AMPs) with tuberculosis-diabetes comorbidity (PTB-DM) is not well understood. METHODS: To study the association of AMPs with PTB-DM, we examined the systemic levels of cathelicidin (LL37), human beta defensin- 2 (HBD2), human neutrophil peptides 1-3, (HNP1-3) and granulysin in individuals with either PTB-DM, PTB, latent TB (LTB) or no TB infection (NTB). RESULTS: Circulating levels of cathelicidin and HBD2 were significantly higher and granulysin levels were significantly lower in PTB-DM compared to PTB, LTB or NTB, while the levels of HNP1-3 were significantly higher in PTB-DM compared to LTB or NTB individuals. Moreover, the levels of cathelicidin and/or HBD2 were significantly higher in PTB-DM or PTB individuals with bilateral and cavitary disease and also exhibited a significant positive relationship with bacterial burden. Cathelidin, HBD2 and HNP1-3 levels exhibited a positive relationship with HbA1c and/or fasting blood glucose levels. Finally, anti-tuberculosis therapy resulted in significantly diminished levels of cathelicidin, HBD2, granulysin and significantly enhanced levels of HNP1-3 and granulysin in PTB-DM and/or PTB individuals. CONCLUSION: Therefore, our data demonstrate that PTB-DM is associated with markedly enhanced levels of AMPs and diminished levels of granulysin.
[Mh] Termos MeSH primário: Peptídeos Catiônicos Antimicrobianos/sangue
Antituberculosos/uso terapêutico
Diabetes Mellitus Tipo 2/metabolismo
Tuberculose Pulmonar/tratamento farmacológico
alfa-Defensinas/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Antígenos de Diferenciação de Linfócitos T/sangue
Catelicidinas/sangue
Comorbidade
Feminino
Seres Humanos
Masculino
Meia-Idade
Tuberculose Pulmonar/metabolismo
Adulto Jovem
beta-Defensinas/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation, T-Lymphocyte); 0 (Antimicrobial Cationic Peptides); 0 (Antitubercular Agents); 0 (Cathelicidins); 0 (DEFB4A protein, human); 0 (GNLY protein, human); 0 (alpha-Defensins); 0 (beta-Defensins); 0 (cathelicidin antimicrobial peptide); 0 (human neutrophil peptide 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184753


  4 / 2165 MEDLINE  
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[PMID]:28886588
[Au] Autor:Cui D; Lyu J; Li H; Lei L; Bian T; Li L; Yan F
[Ad] Endereço:Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, Jiangsu, China.
[Ti] Título:Human ß-defensin 3 inhibits periodontitis development by suppressing inflammatory responses in macrophages.
[So] Source:Mol Immunol;91:65-74, 2017 11.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Human ß-defensin 3 (hBD3) is a cationic peptide with immunomodulatory effects on both innate and acquired immune responses. Periodontitis, an inflammatory disease that extends deep into periodontal tissues, causes the loss of supporting structures around the tooth. The present study assessed the effects of hBD3 as a monotherapy for periodontitis in mice and explored its potential mechanism. In vivo, hBD3 inhibited the levels of tumour necrosis factor (TNF)-α, interleukin-6, and matrix metalloprotease-9 in periodontium exposed to Porphyromonas gingivalis (P.g) in a mouse periodontitis model; reduced osteoclast formation and lower alveolar bone loss were also observed. In addition, hBD3 was related to the expression of polarization signature molecules in circulating monocytes. In vitro, hBD3 notably suppressed the production of TNF-α and interleukin-6 in RAW 264.7 cells stimulated by the lipopolysaccharide of P.g. Moreover, hBD3 attenuated polarization of RAW 264.7 cells into the M1 phenotype, with reduced activation of nuclear factor-κB signal transduction. In conclusion, hBD3 exhibits potent anti-periodontitis properties both in vitro and in vivo, and this effect may be correlated to inhibition of the nuclear factor-κB pathway and macrophage polarization.
[Mh] Termos MeSH primário: Perda do Osso Alveolar/imunologia
Infecções por Bacteroidaceae/imunologia
Osteoclastos/imunologia
Periodontite/imunologia
Porphyromonas gingivalis/imunologia
beta-Defensinas/farmacologia
[Mh] Termos MeSH secundário: Perda do Osso Alveolar/tratamento farmacológico
Perda do Osso Alveolar/genética
Perda do Osso Alveolar/patologia
Animais
Infecções por Bacteroidaceae/tratamento farmacológico
Infecções por Bacteroidaceae/genética
Infecções por Bacteroidaceae/patologia
Modelos Animais de Doenças
Seres Humanos
Interleucina-6/genética
Interleucina-6/imunologia
Masculino
Metaloproteinase 9 da Matriz/genética
Metaloproteinase 9 da Matriz/imunologia
Camundongos
Camundongos Knockout
Osteoclastos/patologia
Periodontite/tratamento farmacológico
Periodontite/genética
Periodontite/patologia
Células RAW 264.7
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-6); 0 (Tumor Necrosis Factor-alpha); 0 (beta-Defensins); 0 (beta-defensin 3, human); 0 (interleukin-6, mouse); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 3.4.24.35 (Mmp9 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE


  5 / 2165 MEDLINE  
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[PMID]:28796463
[Au] Autor:Kim CH; Lee YJ; Go HJ; Oh HY; Lee TK; Park JB; Park NG
[Ad] Endereço:Department of Biotechnology, College of Fisheries Sciences, Pukyong National University, Busan, Korea.
[Ti] Título:Defensin-neurotoxin dyad in a basally branching metazoan sea anemone.
[So] Source:FEBS J;284(19):3320-3338, 2017 Oct.
[Is] ISSN:1742-4658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Recent studies suggest that vertebrate and invertebrate defensins have evolved from two independent ancestors, and that both defensins could share origins with animal toxins. Here, we purified novel sea anemone neurotoxin (BDS)-like antimicrobial peptides (AMPs)-Crassicorin-I and its putative homolog (Crassicorin-II)-from the pharynx extract of an anthozoan sea anemone (Urticina crassicornis). Based on structural analyses and cDNA cloning, mature Crassicorin-I represents a cationic AMP likely generated from a precursor and comprising 40 amino acid residues, including six cysteines forming three intramolecular disulfide bonds. Recombinant Crassicorin-I produced in a heterologous bacterial-expression system displayed antimicrobial activity against both a gram-positive bacterium (Bacillus subtilis) and gram-negative bacteria (Escherichia coli and Salmonella enterica). The Crassicorin-I transcript was upregulated by immune challenge, suggesting its involvement in defense mechanisms against infectious pathogens in sea anemone. Sequence alignment and three-dimensional molecular modeling revealed that Crassicorin-I exhibits high degrees of structural similarity to sea anemone neurotoxins that share ß-defensin fold which is found in vertebrate defensins and invertebrate big-defensins. Consistent with its structural similarity to neurotoxins, Crassicorin-I exhibited paralytic activity toward a crustacean. These findings motivated our investigation and subsequent discovery of antimicrobial activity from other known sea anemone neurotoxins, such as APETx1 and ShK. Collectively, our work signified that Crassicorin-I is the first AMP identified from a sea anemone and provided evidence of a functional linkage between AMPs and neurotoxins in a basally branching metazoan.
[Mh] Termos MeSH primário: Venenos de Cnidários/isolamento & purificação
Neurotoxinas/isolamento & purificação
Anêmonas-do-Mar/química
beta-Defensinas/isolamento & purificação
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Bacillus subtilis/efeitos dos fármacos
Bacillus subtilis/crescimento & desenvolvimento
Sequência de Bases
Clonagem Molecular
Venenos de Cnidários/biossíntese
Venenos de Cnidários/química
Venenos de Cnidários/toxicidade
Sequência Conservada
Escherichia coli/efeitos dos fármacos
Escherichia coli/genética
Escherichia coli/metabolismo
Expressão Gênica
Testes de Sensibilidade Microbiana
Modelos Moleculares
Neurotoxinas/biossíntese
Neurotoxinas/química
Neurotoxinas/toxicidade
Penaeidae/efeitos dos fármacos
Penaeidae/fisiologia
Peptídeos
Domínios e Motivos de Interação entre Proteínas
Estrutura Secundária de Proteína
Proteínas Recombinantes/biossíntese
Proteínas Recombinantes/química
Proteínas Recombinantes/isolamento & purificação
Proteínas Recombinantes/toxicidade
Salmonella enterica/efeitos dos fármacos
Salmonella enterica/crescimento & desenvolvimento
Anêmonas-do-Mar/patogenicidade
Anêmonas-do-Mar/fisiologia
Alinhamento de Sequência
Homologia de Sequência de Aminoácidos
beta-Defensinas/biossíntese
beta-Defensinas/química
beta-Defensinas/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cnidarian Venoms); 0 (Neurotoxins); 0 (Peptides); 0 (Recombinant Proteins); 0 (beta-Defensins); 0 (crassicorin-I, Urticina crassicornis); 0 (crassicorin-II, Urticina crassicornis)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1111/febs.14194


  6 / 2165 MEDLINE  
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[PMID]:28720485
[Au] Autor:Bruno A; Cipollina C; Di Vincenzo S; Siena L; Dino P; Di Gaudio F; Gjomarkaj M; Pace E
[Ad] Endereço:Istituto di Biomedicina e Immunologia Molecolare, Consiglio Nazionale delle Ricerche, Palermo, Italy.
[Ti] Título:Ceftaroline modulates the innate immune and host defense responses of immunocompetent cells exposed to cigarette smoke.
[So] Source:Toxicol Lett;279:9-15, 2017 Sep 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cigarette smoke, the principal risk factor for chronic obstructive pulmonary disease (COPD), negatively influences the effectiveness of the immune system's response to a pathogen. The antibiotic ceftaroline exerts immune-modulatory effects in bronchial epithelial cells exposed to cigarette smoke. AIMS AND METHODS: The present study aims to assess the effects of ceftaroline on TLR2 and TLR4 expression, LPS binding and TNF-α and human beta defensin (HBD2) release in an undifferentiated and PMA-differentiated human monocyte cell line (THP-1) exposed or not to cigarette smoke extracts (CSE). TLR2, TLR4, and LPS binding were assessed by flow cytometry, TNF-α and HBD2 release were evaluated by ELISA. RESULTS: The constitutive expression of TLR2 and TLR4 and LPS binding were higher in differentiated compared to undifferentiated THP-1 cells. In undifferentiated THP-1 cells, CSE increased TLR2 and TLR4 protein levels, LPS binding and TNF-α release and reduced HBD2 release and ceftaroline counteracted all these effects. In differentiated THP-1, CSE did not significantly affect TLR2 and TLR4 expression and LPS binding but reduced HBD2 release and increased TNF-α release. Ceftaroline counteracted the effects of CSE on HBD2 release in differentiated THP-1. CONCLUSION: Ceftaroline counteracts the effect of CSE in immune cells by increasing the effectiveness of the innate immune system. This effect may also assist in reducing pathogen activity and recurrent exacerbations in COPD patients.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Cefalosporinas/farmacologia
Imunidade Inata/efeitos dos fármacos
Imunocompetência
Fatores Imunológicos/farmacologia
Macrófagos/efeitos dos fármacos
Monócitos/efeitos dos fármacos
Fumaça/efeitos adversos
Fumar/efeitos adversos
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Interações Hospedeiro-Patógeno
Seres Humanos
Lipopolissacarídeos/metabolismo
Lipopolissacarídeos/farmacologia
Macrófagos/imunologia
Macrófagos/metabolismo
Monócitos/imunologia
Monócitos/metabolismo
Fumar/imunologia
Receptor 2 Toll-Like/efeitos dos fármacos
Receptor 2 Toll-Like/imunologia
Receptor 2 Toll-Like/metabolismo
Receptor 4 Toll-Like/efeitos dos fármacos
Receptor 4 Toll-Like/imunologia
Receptor 4 Toll-Like/metabolismo
Fator de Necrose Tumoral alfa/imunologia
Fator de Necrose Tumoral alfa/metabolismo
beta-Defensinas/imunologia
beta-Defensinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Cephalosporins); 0 (DEFB4A protein, human); 0 (Immunologic Factors); 0 (Lipopolysaccharides); 0 (Smoke); 0 (T 91825); 0 (TLR2 protein, human); 0 (TLR4 protein, human); 0 (Toll-Like Receptor 2); 0 (Toll-Like Receptor 4); 0 (Tumor Necrosis Factor-alpha); 0 (beta-Defensins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170720
[St] Status:MEDLINE


  7 / 2165 MEDLINE  
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[PMID]:28715972
[Au] Autor:Holly MK; Diaz K; Smith JG
[Ad] Endereço:Department of Microbiology, University of Washington, Seattle, Washington 98195; email: jgsmith2@uw.edu.
[Ti] Título:Defensins in Viral Infection and Pathogenesis.
[So] Source:Annu Rev Virol;4(1):369-391, 2017 Sep 29.
[Is] ISSN:2327-0578
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:α, ß, and θ defensins are effectors of the innate immune system with potent antibacterial, antiviral, and antifungal activity. Defensins have direct antiviral activity in cell culture, with varied mechanisms for individual viruses, although some common themes have emerged. In addition, defensins have potent immunomodulatory activity that can alter innate and adaptive immune responses to viral infection. In some cases, there is evidence for paradoxical escape from defensin neutralization or enhancement of viral infection. The direct and indirect activities of defensins have led to their development as therapeutics and vaccine components. The major area of investigation that continues to lag is the connection between the effects of defensins in cell culture models and viral pathogenesis in vivo. Model systems to study defensin biology, including more physiologic models designed to bridge this gap, are also discussed.
[Mh] Termos MeSH primário: Defensinas/metabolismo
Viroses/imunologia
alfa-Defensinas/metabolismo
beta-Defensinas/metabolismo
[Mh] Termos MeSH secundário: Adenoviridae/efeitos dos fármacos
Adenoviridae/patogenicidade
Animais
Antivirais/farmacologia
Defensinas/genética
Defensinas/farmacologia
Defensinas/uso terapêutico
HIV/efeitos dos fármacos
HIV/patogenicidade
Herpesviridae/efeitos dos fármacos
Herpesviridae/patogenicidade
Seres Humanos
Imunidade Inata
Imunomodulação
Camundongos
Papillomaviridae/efeitos dos fármacos
Papillomaviridae/patogenicidade
Viroses/tratamento farmacológico
alfa-Defensinas/genética
alfa-Defensinas/farmacologia
alfa-Defensinas/uso terapêutico
beta-Defensinas/genética
beta-Defensinas/farmacologia
beta-Defensinas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Defensins); 0 (alpha-Defensins); 0 (beta-Defensins); 0 (theta-defensin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.1146/annurev-virology-101416-041734


  8 / 2165 MEDLINE  
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[PMID]:28708318
[Au] Autor:Chieosilapatham P; Ogawa H; Niyonsaba F
[Ad] Endereço:Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Tokyo, Japan.
[Ti] Título:Current insights into the role of human ß-defensins in atopic dermatitis.
[So] Source:Clin Exp Immunol;190(2):155-166, 2017 Nov.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Anti-microbial peptides or host defence peptides are small molecules that display both anti-microbial activities and complex immunomodulatory functions to protect against various diseases. Among these peptides, the human ß-defensins (hBDs) are localized primarily in epithelial surfaces, including those of the skin, where they contribute to protective barriers. In atopic dermatitis skin lesions, altered skin barrier and immune dysregulation are believed to be responsible for reduced hBD synthesis. Impaired hBD expression in the skin is reportedly the leading cause of increased susceptibility to bacterial and viral infection in patients with atopic dermatitis. Although hBDs have considerable beneficial effects as anti-microbial agents and immunomodulators and may ameliorate atopic dermatitis clinically, recent evidence has also suggested the negative effects of hBDs in atopic dermatitis development. In the current review, we provide an overview of the regulation of hBDs and their role in the pathogenesis of atopic dermatitis. The efforts to utilize these molecules in clinical applications are also described.
[Mh] Termos MeSH primário: Dermatite Atópica/imunologia
beta-Defensinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Dermatite Atópica/fisiopatologia
Dermatite Atópica/terapia
Seres Humanos
Camundongos
beta-Defensinas/biossíntese
beta-Defensinas/genética
beta-Defensinas/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (beta-Defensins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE
[do] DOI:10.1111/cei.13013


  9 / 2165 MEDLINE  
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[PMID]:28694291
[Au] Autor:Gupta K; Idahosa C; Roy S; Lee D; Subramanian H; Dhingra A; Boesze-Battaglia K; Korostoff J; Ali H
[Ad] Endereço:Department of Pathology, University of Pennsylvania School of Dental Medicine, Philadelphia, Pennsylvania, USA.
[Ti] Título:Differential Regulation of Mas-Related G Protein-Coupled Receptor X2-Mediated Mast Cell Degranulation by Antimicrobial Host Defense Peptides and Porphyromonas gingivalis Lipopolysaccharide.
[So] Source:Infect Immun;85(10), 2017 Oct.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:is a keystone pathogen that contributes to periodontal pathogenesis by disrupting host-microbe homeostasis and promoting dysbiosis. The virulence of likely reflects an alteration in the lipid A composition of its lipopolysaccharide (LPS) from the penta-acylated ( LPS ) to the tetra-acylated ( LPS ) form. Mast cells play an important role in periodontitis, but the mechanisms of their activation and regulation remain unknown. The expression of epithelium- and neutrophil-derived host defense peptides (HDPs) (LL-37 and human ß-defensin-3), which activate mast cells via Mas-related G protein-coupled receptor X2 (MRGPRX2), is increased in periodontitis. We found that MRGPRX2-expressing mast cells are present in normal gingiva and that their numbers are elevated in patients with chronic periodontitis. Furthermore, HDPs stimulated degranulation in a human mast cell line (LAD2) and in RBL-2H3 cells stably expressing MRGPRX2 (RBL-MRGPRX2). LPS caused substantial inhibition of HDP-induced mast cell degranulation, but LPS had no effect. A fluorescently labeled HDP (FAM-LL-37) bound to RBL-MRGPRX2 cells, and LPS inhibited this binding, but LPS had no effect. These findings suggest that low-level inflammation induced by HDP/MRGPRX2-mediated mast cell degranulation contributes to gingival homeostasis but that sustained inflammation due to elevated levels of both HDPs and MRGPRX2-expressing mast cells promotes periodontal disease. Furthermore, differential regulation of HDP-induced mast cell degranulation by LPS and LPS may contribute to the modulation of disease progression.
[Mh] Termos MeSH primário: Peptídeos Catiônicos Antimicrobianos/imunologia
Infecções por Bacteroidaceae/imunologia
Degranulação Celular
Periodontite Crônica/imunologia
Lipopolissacarídeos/imunologia
Mastócitos/imunologia
Proteínas do Tecido Nervoso/metabolismo
Receptores Acoplados a Proteínas-G/metabolismo
Receptores de Neuropeptídeos/metabolismo
[Mh] Termos MeSH secundário: Peptídeos Catiônicos Antimicrobianos/química
Peptídeos Catiônicos Antimicrobianos/metabolismo
Linhagem Celular
Periodontite Crônica/microbiologia
Imunofluorescência
Gengiva/imunologia
Gengiva/microbiologia
Gengiva/ultraestrutura
Seres Humanos
Lipopolissacarídeos/metabolismo
Mastócitos/metabolismo
Proteínas do Tecido Nervoso/genética
Porphyromonas gingivalis/química
Porphyromonas gingivalis/imunologia
Porphyromonas gingivalis/metabolismo
Receptores Acoplados a Proteínas-G/genética
Receptores de Neuropeptídeos/genética
beta-Defensinas/genética
beta-Defensinas/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimicrobial Cationic Peptides); 0 (Lipopolysaccharides); 0 (MRGPRX2 protein, human); 0 (Nerve Tissue Proteins); 0 (Receptors, G-Protein-Coupled); 0 (Receptors, Neuropeptide); 0 (beta-Defensins); 0 (beta-defensin 3, human); 143108-26-3 (CAP18 lipopolysaccharide-binding protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE


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[PMID]:28642103
[Au] Autor:Mathew B; Olli S; Guru A; Nagaraj R
[Ad] Endereço:CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad 500 007, India. Electronic address: basil011986@gmail.com.
[Ti] Título:Chimeric analogs of human ß-defensin 1 and θ-defensin disrupt pre-established bacterial biofilms.
[So] Source:Bioorg Med Chem Lett;27(15):3264-3266, 2017 08 01.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Antibiofilm activity of several human defensin analogs that have the ability to kill planktonic bacteria, against pre-established biofilms of Escherichia coli MG1655 and Staphylococcus aureus NCTC 8530 were examined. Linear and linear fatty acylated analogs did not show any activity while disulfide constrained analogs disrupted pre-established S. aureus biofilms. Chimeric analogs of human ß-defensin 1 and θ-defensin, hBTD-1 and [d]hBTD-1 were highly active against S. aureus biofilms. Among the analogs tested, only the d-enantiomer [d]hBTD-1 showed activity against E. coli biofilm. Our study provides insights into the structural requirements for the eradication of pre-established biofilms in defensin analogs.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Biofilmes/efeitos dos fármacos
Defensinas/farmacologia
Escherichia coli/efeitos dos fármacos
Staphylococcus aureus/efeitos dos fármacos
beta-Defensinas/farmacologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Antibacterianos/química
Defensinas/química
Escherichia coli/fisiologia
Infecções por Escherichia coli/microbiologia
Infecções por Escherichia coli/prevenção & controle
Seres Humanos
Infecções Estafilocócicas/microbiologia
Infecções Estafilocócicas/prevenção & controle
Staphylococcus aureus/fisiologia
beta-Defensinas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (DEFB1 protein, human); 0 (Defensins); 0 (beta-Defensins); 0 (theta-defensin)
[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:170624
[St] Status:MEDLINE



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