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[PMID]:29458547
[Au] Autor:Growcott EJ; Bamba D; Galarneau JR; Leonard VHJ; Schul W; Stein D; Osborne CS
[Ad] Endereço:1​Novartis Institutes for Biomedical Research, Infectious Disease, Emeryville, CA, USA.
[Ti] Título:The effect of P38 MAP kinase inhibition in a mouse model of influenza.
[So] Source:J Med Microbiol;67(3):452-462, 2018 Mar.
[Is] ISSN:1473-5644
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Influenza viruses are a common cause of human respiratory infections, resulting in epidemics of high morbidity and mortality. We investigated the effect of a novel mitogen-activated protein kinase (MAPK) inhibitor in vitro and in a murine influenza model to further explore whether p38 MAPK inhibition could reduce viral replication. METHODS: In vitro, the antiviral effect of p38 MAPK inhibitor BCT194 was evaluated in differentiated human bronchial epithelial cells (HBECs); in vivo, female BALB/c mice were infected intranasally with 150 pfu of influenza H1N1 A/Puerto Rico/8/34 and treated with BCT197 (a closely related p38 MAPK inhibitor with an IC50 value of<1 µM, currently in clinical testing), dexamethasone or oseltamivir (Tamiflu) starting 24 h post infection. Body weight, bronchoalveolar lavage cells, cytokines, total protein and lactate dehydrogenase as well as serum cytokines were measured; a subset of animals was evaluated histopathologically.Results/Key findings. p38MAP kinase inhibition with BCT194 had no impact on influenza replication in HBECs. When examining BCT197 in vivo, and comparing to vehicle-treated animals, reduced weight loss, improvement in survival and lack of impaired viral control was observed at BCT197 concentrations relevant to those being used in clinical trials of acute exacerbations of chronic obstructive pulmonary disease; at higher concentrations of BCT197 these effects were reduced. CONCLUSIONS: Compared to vehicle treatment, BCT197 (administered at a clinically relevant concentration) improved outcomes in a mouse model of influenza. This is encouraging given that the use of innate inflammatory pathway inhibitors may raise concerns of negative effects on infection regulation.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Inibidores Enzimáticos/farmacologia
Vírus da Influenza A Subtipo H1N1/efeitos dos fármacos
Infecções por Orthomyxoviridae/virologia
Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Antivirais/administração & dosagem
Antivirais/uso terapêutico
Brônquios/citologia
Linhagem Celular
Citocinas/sangue
Dexametasona/uso terapêutico
Modelos Animais de Doenças
Inibidores Enzimáticos/administração & dosagem
Inibidores Enzimáticos/uso terapêutico
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/virologia
Feminino
Seres Humanos
Vírus da Influenza A Subtipo H1N1/fisiologia
Influenza Humana/tratamento farmacológico
Influenza Humana/virologia
Camundongos
Camundongos Endogâmicos BALB C
Infecções por Orthomyxoviridae/tratamento farmacológico
Oseltamivir/uso terapêutico
Resultado do Tratamento
Replicação Viral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Cytokines); 0 (Enzyme Inhibitors); 20O93L6F9H (Oseltamivir); 7S5I7G3JQL (Dexamethasone); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180221
[St] Status:MEDLINE
[do] DOI:10.1099/jmm.0.000684


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[PMID]:28470141
[Au] Autor:Leslie LJ; Vasanthi Bathrinarayanan P; Jackson P; Mabiala Ma Muanda JA; Pallett R; Stillman CJP; Marshall LJ
[Ad] Endereço:a School of Engineering and Applied Science , Aston University , Birmingham , UK.
[Ti] Título:A comparative study of electronic cigarette vapor extracts on airway-related cell lines in vitro.
[So] Source:Inhal Toxicol;29(3):126-136, 2017 02.
[Is] ISSN:1091-7691
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The use of electronic cigarettes (ECs) is rapidly increasing worldwide; however, scientific evidence regarding EC cytotoxicity is limited. The aim of this study was to evaluate the acute cytotoxicity of EC vapor extract (ECE) on airway-related cells in vitro. Cigarette smoke extract (CSE), vapor extract of fifteen brands/flavors of ECs and the extract from the E-vehicle (propylene glycol and glycerin) was collected. Extracts, in concentrations of 100-12.5%, were added to human bronchial epithelial (BEAS-2B, IB3-1 and C38), fibroblast (Wi-38) and macrophage (J774 and THP-1) cell lines. Viability was assessed after 24 h using a standard XTT assay. Viability of <70% of control (no extract) was considered cytotoxic according to UNI EN ISO 10993-5 standards. CSE displayed a concentration-dependent influence on cell viability across all four cell lines with 100% producing the most toxic effect, therefore validating the model and indicating higher cytotoxicity than in ECEs. ECEs did reduce viability although this was not correlated with nicotine content or the E-vehicle. However, several flavors proved cytotoxic, with variation between different brands and cell lines. These data indicate that not all ECs are the same and that use of a particular flavor or brand may have differing effects. The cell line used is also an important factor. More research is crucial to ascertain the health effects of different ECs before they can be accepted as a safe alternative to tobacco cigarettes.
[Mh] Termos MeSH primário: Misturas Complexas/toxicidade
Sistemas Eletrônicos de Liberação de Nicotina
Aromatizantes/toxicidade
Fumaça
[Mh] Termos MeSH secundário: Brônquios/citologia
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Seres Humanos
Macrófagos/efeitos dos fármacos
Nicotina/toxicidade
Tabaco
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Complex Mixtures); 0 (Flavoring Agents); 0 (Smoke); 6M3C89ZY6R (Nicotine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1080/08958378.2017.1318193


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[PMID]:28464886
[Au] Autor:Yeo J; Crawford EL; Zhang X; Khuder S; Chen T; Levin A; Blomquist TM; Willey JC
[Ad] Endereço:Division of Pulmonary and Critical Care Medicine, Department of Medicine, The University of Toledo College of Medicine, 3000 Arlington Avenue, HEB 219, Toledo, OH, 43614, USA.
[Ti] Título:A lung cancer risk classifier comprising genome maintenance genes measured in normal bronchial epithelial cells.
[So] Source:BMC Cancer;17(1):301, 2017 May 02.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Annual low dose CT (LDCT) screening of individuals at high demographic risk reduces lung cancer mortality by more than 20%. However, subjects selected for screening based on demographic criteria typically have less than a 10% lifetime risk for lung cancer. Thus, there is need for a biomarker that better stratifies subjects for LDCT screening. Toward this goal, we previously reported a lung cancer risk test (LCRT) biomarker comprising 14 genome-maintenance (GM) pathway genes measured in normal bronchial epithelial cells (NBEC) that accurately classified cancer (CA) from non-cancer (NC) subjects. The primary goal of the studies reported here was to optimize the LCRT biomarker for high specificity and ease of clinical implementation. METHODS: Targeted competitive multiplex PCR amplicon libraries were prepared for next generation sequencing (NGS) analysis of transcript abundance at 68 sites among 33 GM target genes in NBEC specimens collected from a retrospective cohort of 120 subjects, including 61 CA cases and 59 NC controls. Genes were selected for analysis based on contribution to the previously reported LCRT biomarker and/or prior evidence for association with lung cancer risk. Linear discriminant analysis was used to identify the most accurate classifier suitable to stratify subjects for screening. RESULTS: After cross-validation, a model comprising expression values from 12 genes (CDKN1A, E2F1, ERCC1, ERCC4, ERCC5, GPX1, GSTP1, KEAP1, RB1, TP53, TP63, and XRCC1) and demographic factors age, gender, and pack-years smoking, had Receiver Operator Characteristic area under the curve (ROC AUC) of 0.975 (95% CI: 0.96-0.99). The overall classification accuracy was 93% (95% CI 88%-98%) with sensitivity 93.1%, specificity 92.9%, positive predictive value 93.1% and negative predictive value 93%. The ROC AUC for this classifier was significantly better (p < 0.0001) than the best model comprising demographic features alone. CONCLUSIONS: The LCRT biomarker reported here displayed high accuracy and ease of implementation on a high throughput, quality-controlled targeted NGS platform. As such, it is optimized for clinical validation in specimens from the ongoing LCRT blinded prospective cohort study. Following validation, the biomarker is expected to have clinical utility by better stratifying subjects for annual lung cancer screening compared to current demographic criteria alone.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/análise
Brônquios/citologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/metabolismo
[Mh] Termos MeSH secundário: Antioxidantes/análise
Antioxidantes/metabolismo
Biomarcadores Tumorais/genética
Biomarcadores Tumorais/metabolismo
Biópsia
Brônquios/metabolismo
Células Epiteliais/citologia
Células Epiteliais/metabolismo
Seres Humanos
Neoplasias Pulmonares/diagnóstico
Neoplasias Pulmonares/epidemiologia
Reação em Cadeia da Polimerase
Curva ROC
Reprodutibilidade dos Testes
Estudos Retrospectivos
Medição de Risco
Tomografia Computadorizada Espiral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Biomarkers, Tumor)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12885-017-3287-4


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[PMID]:29465555
[Au] Autor:Sheth HS; Maldonado F; Lentz RJ
[Ad] Endereço:D. Y. Patil University School of Medicine, Mumbai, India.
[Ti] Título:Two cases of Dieulafoy lesions of the bronchus with novel comorbid associations and endobronchial ablative management.
[So] Source:Medicine (Baltimore);97(8):e9754, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Dieulafoy lesions are aberrantly large submucosal arteries most frequently associated with gastrointestinal hemorrhage. They are rarely identified in the bronchial submucosa and can cause massive hemoptysis. PATIENT CONCERNS: We present three episodes of massive hemoptysis in two patients, the first with comorbid Alagille syndrome including multiple cardiac and pulmonary vascular abnormalities and the second with thyroid cancer metastatic to the mediastinum. DIAGNOSES: All episodes were due to Dieulafoy lesions of the bronchus based on bronchoscopic appearance. INTERVENTIONS: Bronchoscopic ablation using Nd:YAP laser was attempted both patients. OUTCOMES: Nd:YAP laser successfully ablated the Dieulafoy lesion in the first case with long-term relief from recurrent hemoptysis. The first episode in the second patient responded to bronchial artery embolization; laser ablation of a different Dieulafoy lesion responsible for the second episode was unsuccessful but additional bronchial artery embolization has provided relief from further episodes. LESSONS: Bronchoscopic ablation of Dieulafoy lesions of the bronchus can provide durable relief from recurrent symptoms. Clinical and anatomical features should be considered carefully before intervention, which should only be attempted by experienced operators with appropriate ancillary support available.
[Mh] Termos MeSH primário: Técnicas de Ablação/métodos
Broncopatias/cirurgia
Broncoscopia/métodos
Hemoptise/cirurgia
Malformações Vasculares/cirurgia
[Mh] Termos MeSH secundário: Idoso
Síndrome de Alagille/patologia
Brônquios/irrigação sanguínea
Brônquios/cirurgia
Broncopatias/complicações
Comorbidade
Feminino
Hemoptise/etiologia
Seres Humanos
Masculino
Neoplasias do Mediastino/secundário
Meia-Idade
Neoplasias da Glândula Tireoide/patologia
Malformações Vasculares/complicações
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180222
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009754


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[PMID]:29428600
[Au] Autor:Yao ZH; Xie HJ; Yuan YL; Huo YT; Cao J; Lai WY; Cai RJ; Cheng YX
[Ad] Endereço:Department of Respiratory Disease, Academy of Orthopedics of Guangdong Province, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; Department of Respiratory Disease, Hengyang NO.1 Peoples Hospital, Hengyang, Hunan, China.
[Ti] Título:Contraction-dependent TGF-ß1 activation is required for thrombin-induced remodeling in human airway smooth muscle cells.
[So] Source:Life Sci;197:130-139, 2018 Mar 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Thrombin is a serine proteinase that is not only involved in coagulation cascade, but also mediates a number of biological responses relevant to tissues repair, and induces bronchoconstriction. TGF-ß plays a pivotal role in airway remodeling due to its effects on airway smooth muscle proliferation and extracellular matrix (ECM) deposition. Recently, bronchoconstriction itself is found to constitute a form of strain and is highly relevant to asthmatic airway remodeling. However, the underlying mechanisms remain unknown. Here, we investigated the role of contraction- dependent TGF-ß activation in thrombin-induced remodeling in human airway smooth muscle (HASM) cells. MATERIALS AND METHODS: Primary HASM cells were treated with or without thrombin in the absence or presence of anti-TGF-ß antibody, cytochalasin D and formoterol. CFSE labeling index or CCK-8 assay were performed to test cell proliferation. RT-PCR and Western blotting were used to examined ECM mRNA level and collagen Iα1, α-actin protein expression, respectively. Immunofluorescence was also used to confirm contraction induced by thrombin in HASM cells. KEY FINDING: Thrombin stimulation enhanced HASM cells proliferation and activated TGF-ß signaling. Thrombin induced ECM mRNA and collagen Iα1 protein expression, and these effects are mediated by TGF-ß. Abrogation of TGF-ß activation by contraction inhibitors cytochalasin D and formoterol prevents the thrombin-induced effects. SIGNIFICANCE: These findings suggest that contraction-dependent TGF-ß activation could be a mechanism by which thrombin leads to the development of asthmatic airway remodeling. Blocking physical forces with bronchodilator would be an intriguing way in reducing airway remodeling in asthma.
[Mh] Termos MeSH primário: Remodelação das Vias Aéreas/efeitos dos fármacos
Brônquios/metabolismo
Proliferação Celular/efeitos dos fármacos
Miócitos de Músculo Liso/metabolismo
Transdução de Sinais/efeitos dos fármacos
Trombina/farmacologia
Fator de Crescimento Transformador beta1/metabolismo
[Mh] Termos MeSH secundário: Brônquios/patologia
Células Cultivadas
Seres Humanos
Miócitos de Músculo Liso/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (TGFB1 protein, human); 0 (Transforming Growth Factor beta1); EC 3.4.21.5 (Thrombin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180212
[St] Status:MEDLINE


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[PMID]:29360847
[Au] Autor:Sutanto EN; Scaffidi A; Garratt LW; Looi K; Foo CJ; Tessari MA; Janssen RA; Fischer DF; Stick SM; Kicic A; AREST CF
[Ad] Endereço:Telethon Kids Institute, the University of Western Australia, Nedlands, Western Australia, Australia.
[Ti] Título:Assessment of p.Phe508del-CFTR functional restoration in pediatric primary cystic fibrosis airway epithelial cells.
[So] Source:PLoS One;13(1):e0191618, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Mutations in the cystic fibrosis transmembrane regulator (CFTR) gene can reduce function of the CFTR ion channel activity and impair cellular chloride secretion. The gold standard method to assess CFTR function of ion transport using the Ussing chamber requires a high number of airway epithelial cells grown at air-liquid interface, limiting the application of this method for high throughput screening of potential therapeutic compounds in primary airway epithelial cells (pAECs) featuring less common CFTR mutations. This study assessed an alternative approach, using a small scale halide assay that can be adapted for a personalized high throughput setting to analyze CFTR function of pAEC. METHODS: Pediatric pAECs derived from children with CF (pAECCF) were established and expanded as monolayer cultures, before seeding into 96-well plates for the halide assay. Cells were then transduced with an adenoviral construct containing yellow fluorescent protein (eYFP) reporter gene, alone or in combination with either wild-type CFTR (WT-CFTR) or p.Phe508del CFTR. Four days post transduction, cells were stimulated with forskolin and genistein, and assessed for quenching of the eYFP signal following injection of iodide solution into the assay media. RESULTS: Data showed that pAECCF can express eYFP at high efficiency following transduction with the eYFP construct. The halide assay was able to discriminate functional restoration of CFTR in pAECCF treated with either WT-CFTR construct or the positive controls syntaxin 8 and B-cell receptor-associated protein 31 shRNAs. SIGNIFICANCE: The current study demonstrates that the halide assay can be adapted for pediatric pAECCF to evaluate restoration of CFTR function. With the ongoing development of small molecules to modulate the folding and/or activity of various mutated CFTR proteins, this halide assay presents a small-scale personalized screening platform that could assess therapeutic potential of molecules across a broad range of CFTR mutations.
[Mh] Termos MeSH primário: Brônquios/metabolismo
Regulador de Condutância Transmembrana em Fibrose Cística/fisiologia
Fibrose Cística/fisiopatologia
Fenilalanina/química
Traqueia/metabolismo
[Mh] Termos MeSH secundário: Adenoviridae/genética
Brônquios/citologia
Células Cultivadas
Criança
Fibrose Cística/patologia
Regulador de Condutância Transmembrana em Fibrose Cística/química
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Células Epiteliais/metabolismo
Vetores Genéticos
Seres Humanos
Transporte Proteico
Traqueia/citologia
Transdução Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 47E5O17Y3R (Phenylalanine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191618


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[PMID]:28464879
[Au] Autor:Kainuma K; Kobayashi T; D'Alessandro-Gabazza CN; Toda M; Yasuma T; Nishihama K; Fujimoto H; Kuwabara Y; Hosoki K; Nagao M; Fujisawa T; Gabazza EC
[Ad] Endereço:Allergy Center, Mie National Hospital, 357 Osato-kubota, Tsu, Mie, 514-0125, Japan.
[Ti] Título:ß adrenergic agonist suppresses eosinophil-induced epithelial-to-mesenchymal transition of bronchial epithelial cells.
[So] Source:Respir Res;18(1):79, 2017 May 02.
[Is] ISSN:1465-993X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Epithelial-mesenchymal transition is currently recognized as an important mechanism for the increased number of myofibroblasts in cancer and fibrotic diseases. We have already reported that epithelial-mesenchymal transition is involved in airway remodeling induced by eosinophils. Procaterol is a selective and full ß adrenergic agonist that is used as a rescue of asthmatic attack inhaler form and orally as a controller. In this study, we evaluated whether procaterol can suppress epithelial-mesenchymal transition of airway epithelial cells induced by eosinophils. METHODS: Epithelial-mesenchymal transition was assessed using a co-culture system of human bronchial epithelial cells and primary human eosinophils or an eosinophilic leukemia cell line. RESULTS: Procaterol significantly inhibited co-culture associated morphological changes of bronchial epithelial cells, decreased the expression of vimentin, and increased the expression of E-cadherin compared to control. Butoxamine, a specific ß -adrenergic antagonist, significantly blocked changes induced by procaterol. In addition, procaterol inhibited the expression of adhesion molecules induced during the interaction between eosinophils and bronchial epithelial cells, suggesting the involvement of adhesion molecules in the process of epithelial-mesenchymal transition. Forskolin, a cyclic adenosine monophosphate-promoting agent, exhibits similar inhibitory activity of procaterol. CONCLUSIONS: Overall, these observations support the beneficial effect of procaterol on airway remodeling frequently associated with chronic obstructive pulmonary diseases.
[Mh] Termos MeSH primário: Eosinófilos/fisiologia
Células Epiteliais/citologia
Células Epiteliais/fisiologia
Transição Epitelial-Mesenquimal/fisiologia
Procaterol/administração & dosagem
Mucosa Respiratória/citologia
Mucosa Respiratória/fisiologia
[Mh] Termos MeSH secundário: Agonistas de Receptores Adrenérgicos beta 2/administração & dosagem
Brônquios/citologia
Brônquios/diagnóstico por imagem
Brônquios/fisiologia
Linhagem Celular
Relação Dose-Resposta a Droga
Eosinófilos/citologia
Eosinófilos/efeitos dos fármacos
Células Epiteliais/efeitos dos fármacos
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Seres Humanos
Mucosa Respiratória/efeitos dos fármacos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-2 Receptor Agonists); X7I3EMM5K0 (Procaterol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12931-017-0563-4


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[PMID]:29286858
[Au] Autor:Ritchie AI; Singanayagam A; Wiater E; Edwards MR; Montminy M; Johnston SL
[Ad] Endereço:1 National Heart and Lung Institute, Imperial College London, United Kingdom.
[Ti] Título:ß -Agonists Enhance Asthma-Relevant Inflammatory Mediators in Human Airway Epithelial Cells.
[So] Source:Am J Respir Cell Mol Biol;58(1):128-132, 2018 01.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Agonistas de Receptores Adrenérgicos beta 2/farmacologia
Asma/metabolismo
Brônquios/metabolismo
Células Epiteliais/metabolismo
Mediadores da Inflamação/metabolismo
[Mh] Termos MeSH secundário: Asma/patologia
Fator Neurotrófico Derivado do Encéfalo/biossíntese
Brônquios/patologia
Linhagem Celular
Células Epiteliais/patologia
Seres Humanos
Interleucina-11/biossíntese
Interleucina-6/biossíntese
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
0 (Adrenergic beta-2 Receptor Agonists); 0 (Brain-Derived Neurotrophic Factor); 0 (IL11 protein, human); 0 (IL6 protein, human); 0 (Inflammation Mediators); 0 (Interleukin-11); 0 (Interleukin-6); 0 (brain-derived neurotrophic factor, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2017-0315LE


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[PMID]:29309811
[Au] Autor:Park EJ; Park SJ; Kim S; Lee K; Chang J
[Ad] Endereço:Graduate school of East-West Medical Science, Kyung Hee University, Yongin-si, Gyeonggi-do, 17104, Republic of Korea. Electronic address: pejtoxic@hanmail.net.
[Ti] Título:Lung fibroblasts may play an important role in clearing apoptotic bodies of bronchial epithelial cells generated by exposure to PHMG-P-containing solution.
[So] Source:Toxicol Lett;286:108-119, 2018 Apr.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Polyhexamethylene guanidine (PHMG) has been widely used in the industry owing to its excellent biocidal, anti-corrosive, and anti-biofouling properties. In Korea, consumers exposed to PHMG-phosphate (PHMG-P)-containing humidifier disinfectant have begun to suffer from fibrotic lung injury-related symptoms for unknown reasons. However, no appropriate treatment has yet been found because the detail toxic mechanism has not been identified. Herein, we first studied the toxic mechanism of PHMG-P-containing solution using human normal bronchial epithelial cells (BEAS-2B cells). When exposed for 24 h, PHMG-P-containing solution rapidly decreased cell viability from around 6 h after exposure and significantly increased of the phosphatidylserine exposure and the LDH release. At 6 h of exposure, the material contained in the solution was found to be bound to the cell membrane and the inner wall of vacuoles, and damaged the cell membrane and organelles. In addition, a significant increase of IFN-γ was observed among cytokines, the expression of apoptosis-, autophagy-, and membrane and DNA damage-related proteins was also enhanced. Meanwhile, the level of intracellular ROS and the secretion of IL-8 and CXCL-1, which are chemokines for professional phagocytes, decreased. Thus, we treated dead BEAS-2B cells to lung fibroblasts (HFL-1), non-professional phagocytes, and then we observed that the dead cells rapidly attached to HFL-1 cells and were taken up. Additionally, increased secretion of IL-8 and CXCL-1 was observed in the cells. Based on these results, we suggest that pulmonary exposure to PHMG-P induces apoptosis of bronchial epithelial cells and lung fibroblasts might play an important role in the clearance of the apoptotic debris.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Brônquios/efeitos dos fármacos
Citofagocitose
Desinfetantes/toxicidade
Células Epiteliais/efeitos dos fármacos
Fibroblastos/metabolismo
Guanidinas/toxicidade
[Mh] Termos MeSH secundário: Brônquios/metabolismo
Brônquios/ultraestrutura
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Quimiocina CXCL1/metabolismo
Relação Dose-Resposta a Droga
Células Epiteliais/metabolismo
Células Epiteliais/ultraestrutura
Fibroblastos/ultraestrutura
Seres Humanos
Interferon gama/metabolismo
Interleucina-8/metabolismo
L-Lactato Desidrogenase/metabolismo
Fosfatidilserinas/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL1 protein, human); 0 (Chemokine CXCL1); 0 (Disinfectants); 0 (Guanidines); 0 (IFNG protein, human); 0 (IL8 protein, human); 0 (Interleukin-8); 0 (Phosphatidylserines); 31961-54-3 (polyhexamethyleneguanidine); 82115-62-6 (Interferon-gamma); EC 1.1.1.27 (L-Lactate Dehydrogenase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE


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[PMID]:28448456
[Au] Autor:Othumpangat S; Bryan NB; Beezhold DH; Noti JD
[Ad] Endereço:Allergy and Clinical Immunology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, WV 26505, USA. seo8@cdc.gov.
[Ti] Título:Upregulation of miRNA-4776 in Influenza Virus Infected Bronchial Epithelial Cells Is Associated with Downregulation of NFKBIB and Increased Viral Survival.
[So] Source:Viruses;9(5), 2017 04 27.
[Is] ISSN:1999-4915
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Influenza A virus (IAV) infection remains a significant cause of morbidity and mortality worldwide. One key transcription factor that is activated upon IAV infection is nuclear factor Kappa B (NF-κB). NF-κB regulation involves the inhibitor proteins NF-κB inhibitor beta (NFKBIB), (also known as IκB ß), which form complexes with NF-κB to sequester it in the cytoplasm. In this study, microarray data showed differential expression of several microRNAs (miRNAs) on exposure to IAV. Target scan analysis revealed that miR-4776, miR-4514 and miR-4742 potentially target NFKBIB messenger RNA (mRNA). Time-course analysis of primary bronchial epithelial cells (HBEpCs) showed that miR-4776 expression is increased within 1 h of infection, followed by its downregulation 4 h post-exposure to IAV. NFKBIB upregulation of miR-4776 correlated with a decrease in NFKBIB expression within 1 h of infection and a subsequent increase in NFKBIB expression 4 h post-infection. In addition, miRNA ago-immunoprecipitation studies and the three prime untranslated region (3' UTR) luciferase assay confirmed that miR-4776 targets NFKBIB mRNA. Furthermore, uninfected HBEpCs transfected with miR-4776 mimic showed decreased expression of NFKBIB mRNA. Overexpression of NFKBIB protein in IAV infected cells led to lower levels of IAV. Taken together, our data suggest that miRNA-4776 modulates IAV production in infected cells through NFKBIB expression, possibly through the modulation of NF-κB.
[Mh] Termos MeSH primário: Brônquios/virologia
Células Epiteliais/virologia
Proteínas I-kappa B/genética
Vírus da Influenza A Subtipo H1N1/fisiologia
MicroRNAs/genética
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Brônquios/citologia
Linhagem Celular
Regulação para Baixo
Regulação da Expressão Gênica
Seres Humanos
Proteínas I-kappa B/metabolismo
Análise em Microsséries
Viabilidade Microbiana
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Transdução de Sinais
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (I kappa B beta protein); 0 (I-kappa B Proteins); 0 (MicroRNAs); 0 (RNA, Messenger)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE



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