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  1 / 1564 MEDLINE  
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[PMID]:29268133
[Au] Autor:Zhu G; Xu Y; Cen X; Nandakumar KS; Liu S; Cheng K
[Ad] Endereço:Guangdong Provincial Key Laboratory of New Drug Screening and Guangzhou Key Laboratory of Drug Research for Emerging Virus Prevention and Treatment, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, 510515, China.
[Ti] Título:Targeting pattern-recognition receptors to discover new small molecule immune modulators.
[So] Source:Eur J Med Chem;144:82-92, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Pattern recognition receptors (PRRs) are key immune receptors of the innate immune system, which recognize the conserved pathogen-associated molecular patterns (PAMPs) of the invading pathogens. Compared to the adaptive immune receptors, PRRs have three distinguishing features, viz., universal expression, fast response and recognizing many kinds of microbes. Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), C-type lectin receptors (CLRs) and NOD-like receptors (NLRs) recognize viral nucleic acid/bacterial fragments and trigger anti-microbial innate immune responses. Upon recognition of their ligand species, PRRs recruit specific intracellular adaptor proteins to initiate signaling pathways culminating in the activation of nuclear factor-κB (NF-κB), mitogen-activated protein (MAP) kinases and interferon regulatory factors (IRFs) that control the transcription of genes encoding pro-inflammatory factors including type I interferon and other inflammatory cytokines, which are critical for eliminating the potential threat to the host. Here, we summarize the effects of small molecule regulators acting on signaling pathways initiated by TLR, RLR and NLR as well as their influence on innate and adaptive immune responses leading to therapy.
[Mh] Termos MeSH primário: Imunidade Adaptativa/efeitos dos fármacos
Imunidade Inata/efeitos dos fármacos
Fatores Imunológicos/química
Fatores Imunológicos/farmacologia
Receptores de Reconhecimento de Padrão/imunologia
[Mh] Termos MeSH secundário: Animais
Descoberta de Drogas
Seres Humanos
Inflamação/tratamento farmacológico
Inflamação/imunologia
Terapia de Alvo Molecular
Bibliotecas de Moléculas Pequenas/química
Bibliotecas de Moléculas Pequenas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Immunologic Factors); 0 (Receptors, Pattern Recognition); 0 (Small Molecule Libraries)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


  2 / 1564 MEDLINE  
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[PMID]:28458047
[Au] Autor:Yasuda S; Okada K; Saijo Y
[Ad] Endereço:Graduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma 630-0192, Japan.
[Ti] Título:A look at plant immunity through the window of the multitasking coreceptor BAK1.
[So] Source:Curr Opin Plant Biol;38:10-18, 2017 08.
[Is] ISSN:1879-0356
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Recognition of microbe- and danger-associated molecular patterns (MAMPs and DAMPs, respectively) by pattern recognition receptors (PRRs) is central to innate immunity in both plants and animals. The plant PRRs described to date are all cell surface-localized receptors. According to their ligand-binding ectodomains, each PRR engages a specific coreceptor or adaptor kinase in its signaling complexes to regulate defense signaling. With a focus on the coreceptor RLK BRI1-ASSOCIATED RECEPTOR KINASE1 (BAK1) and related SOMATIC EMBRYOGENESIS RECEPTOR KINASEs (SERKs), here we review the increasing inventory of BAK1 partners and their functions in plant immunity. We also discuss the significance of autoimmunity triggered by BAK1/SERK4 disintegration in shaping the strategies for attenuation of PRR signaling by infectious microbes and host plants.
[Mh] Termos MeSH primário: Proteínas de Arabidopsis/imunologia
Proteínas de Arabidopsis/metabolismo
Arabidopsis/imunologia
[Mh] Termos MeSH secundário: Arabidopsis/metabolismo
Proteínas de Arabidopsis/genética
Imunidade Vegetal/genética
Imunidade Vegetal/fisiologia
Proteínas Serina-Treonina Quinases/genética
Proteínas Serina-Treonina Quinases/metabolismo
Receptores de Reconhecimento de Padrão/genética
Receptores de Reconhecimento de Padrão/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Arabidopsis Proteins); 0 (Receptors, Pattern Recognition); EC 2.7.1.- (BAK1 protein, Arabidopsis); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


  3 / 1564 MEDLINE  
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[PMID]:28462528
[Au] Autor:Tonnus W; Linkermann A
[Ad] Endereço:Division of Nephrology, Department of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universität Dresden, Dresden, Germany.
[Ti] Título:The in vivo evidence for regulated necrosis.
[So] Source:Immunol Rev;277(1):128-149, 2017 05.
[Is] ISSN:1600-065X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Necrosis is a hallmark of several widespread diseases or their direct complications. In the past decade, we learned that necrosis can be a regulated process that is potentially druggable. RIPK3- and MLKL-mediated necroptosis represents by far the best studied pathway of regulated necrosis. During necroptosis, the release of damage-associated molecular patterns (DAMPs) drives a phenomenon referred to as necroinflammation, a common consequence of necrosis. However, most studies of regulated necrosis investigated cell lines in vitro in a cell autonomous manner, which represents a non-physiological situation. Conclusions based on such work might not necessarily be transferrable to disease states in which synchronized, non-cell autonomous effects occur. Here, we summarize the current knowledge of the pathophysiological relevance of necroptosis in vivo, and in light of this understanding, we reassess the morphological classification of necrosis that is generally used by pathologists. Along these lines, we discuss the paucity of data implicating necroptosis in human disease. Finally, the in vivo relevance of non-necroptotic forms of necrosis, such as ferroptosis, is addressed.
[Mh] Termos MeSH primário: Inflamação
Ferro/metabolismo
Necrose
[Mh] Termos MeSH secundário: Animais
Microambiente Celular
Colágeno
Seres Humanos
Proteínas Quinases/metabolismo
Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo
Receptores de Reconhecimento de Padrão/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Pattern Recognition); 9007-34-5 (Collagen); E1UOL152H7 (Iron); EC 2.7.- (MLKL protein, human); EC 2.7.- (Protein Kinases); EC 2.7.11.1 (RIPK3 protein, human); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases)
[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:170503
[St] Status:MEDLINE
[do] DOI:10.1111/imr.12551


  4 / 1564 MEDLINE  
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[PMID]:28462521
[Au] Autor:Orozco S; Oberst A
[Ad] Endereço:Department of Immunology, University of Washington, Seattle, WA, USA.
[Ti] Título:RIPK3 in cell death and inflammation: the good, the bad, and the ugly.
[So] Source:Immunol Rev;277(1):102-112, 2017 05.
[Is] ISSN:1600-065X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Necroptosis is a form of cell death that can be observed downstream of death receptor or pattern recognition receptor signaling under certain cellular contexts, or in response to some viral and bacterial infections. The receptor interacting protein kinases-1 (RIPK1) and RIPK3 are at the core of necroptotic signaling, among other proteins. Because this pathway is normally halted by the pro-apoptotic protease caspase-8 and the IAP ubiquitin ligases, how and when necroptosis is triggered in physiological settings are ongoing questions. Interestingly, accumulating evidence suggests that RIPK3 has functions beyond the induction of necroptotic cell death, especially in the areas of tissue injury and sterile inflammation. Here, we will discuss the role of RIPK3 in a variety of physiological conditions, including necroptotic and non-necroptotic cell death, in the context of viral and bacterial infections, tissue damage, and inflammation.
[Mh] Termos MeSH primário: Infecções Bacterianas/imunologia
Inflamação/imunologia
Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo
Viroses/imunologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Degradação Necrótica do DNA
Seres Humanos
Necrose
Receptores de Morte Celular/metabolismo
Receptores de Reconhecimento de Padrão/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Receptors, Death Domain); 0 (Receptors, Pattern Recognition); EC 2.7.11.1 (RIPK3 protein, human); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases)
[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:170503
[St] Status:MEDLINE
[do] DOI:10.1111/imr.12536


  5 / 1564 MEDLINE  
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[PMID]:28460048
[Au] Autor:Kolar SS; Baidouri H; McDermott AM
[Ad] Endereço:The Ocular Surface Institute, University of Houston, College of Optometry, Houston, Texas, United States.
[Ti] Título:Role of Pattern Recognition Receptors in the Modulation of Antimicrobial Peptide Expression in the Corneal Epithelial Innate Response to F. solani.
[So] Source:Invest Ophthalmol Vis Sci;58(5):2463-2472, 2017 05 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: Fusarium solani (F. solani) keratitis is a potentially sight-threatening fungal infection of the cornea. Antimicrobial peptides (AMPs), such as human ß-defensins (hBDs) and cathelicidins, essential components of the immune system, likely have a protective role against F. solani keratitis. We examined the role of pattern recognition receptors (PRRs), Dectin-1, and TLR2 in F. solani-induced modulation of AMP expression in vitro. Methods: Human corneal epithelial cells (HCECs) were exposed to heat-inactivated F. solani or pathogen-associated molecular patterns (PAMPs) of F. solani (Zymosan or Zymosan Depleted) for 6, 12, or 24 hours following which AMP mRNA and protein levels were determined. Involvement of TLR2 and Dectin-1 was confirmed by using siRNA knock-down (TLR2 and Dectin-1) or chemical inhibitor BAY 61-3606 (Dectin-1). The functional significance of AMP upregulation was tested using culture supernatant from F. solani or PAMP-treated HCECs against F. solani in the presence of hBD2 or LL37 neutralizing antibody. Results: We confirm that HCECs express Dectin-1 and TLR2. HCECs demonstrated upregulation of AMPs hBD2 and cathelicidin LL37 following exposure to heat-inactivated F. solani or PAMPs. TLR2 and Dectin-1 knockdown and BAY 61-3606 treatment decreased AMP mRNA upregulation confirming PRR involvement. The culture supernatant from F. solani or PAMP-treated HCECs showed substantial killing of F. solani and hBD2 or LL37 neutralizing antibody significantly decreased this effect implicating involvement of these AMPs. Conclusions: These findings demonstrate that Dectin-1 and TLR2 have an important role in regulating F. solani-induced AMP expression in corneal epithelial cells.
[Mh] Termos MeSH primário: Peptídeos Catiônicos Antimicrobianos/genética
Epitélio Anterior/metabolismo
Infecções Oculares Fúngicas/metabolismo
Fusariose/metabolismo
Regulação da Expressão Gênica
Ceratite/metabolismo
Receptores de Reconhecimento de Padrão/genética
[Mh] Termos MeSH secundário: Peptídeos Catiônicos Antimicrobianos/biossíntese
Células Cultivadas
Córnea/metabolismo
Córnea/patologia
Epitélio Anterior/microbiologia
Epitélio Anterior/patologia
Infecções Oculares Fúngicas/imunologia
Citometria de Fluxo
Fusariose/diagnóstico
Fusariose/microbiologia
Seres Humanos
Immunoblotting
Ceratite/diagnóstico
Ceratite/microbiologia
RNA/genética
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Receptores de Reconhecimento de Padrão/metabolismo
Transdução de Sinais
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antimicrobial Cationic Peptides); 0 (RNA, Messenger); 0 (Receptors, Pattern Recognition); 63231-63-0 (RNA)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180124
[Lr] Data última revisão:
180124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.16-20658


  6 / 1564 MEDLINE  
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[PMID]:28744851
[Au] Autor:Zhou Y; He C; Wang L; Ge B
[Ad] Endereço:Shanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
[Ti] Título:Post-translational regulation of antiviral innate signaling.
[So] Source:Eur J Immunol;47(9):1414-1426, 2017 09.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The innate immune system initiates immune responses by pattern-recognition receptors (PRR). Virus-derived nucleic acids are sensed by the retinoic acid-inducible gene I (RIG-I)-like receptor (RLR) family and the toll-like receptor (TLR) family as well as the DNA sensor cyclic GMP-AMP (cGAMP) synthase (cGAS). These receptors activate IRF3/7 and NF-κB signaling pathways to induce the expression of type I interferons (IFNs) and other cytokines firing antiviral responses within the cell. However, to achieve a favorable outcome for the host, a balanced production of IFNs and activation of antiviral responses is required. Post-translational modifications (PTMs), such as the covalent linkage of functional groups to amino acid chains, are crucial for this immune homeostasis in antiviral responses. Canonical PTMs including phosphorylation and ubiquitination have been extensively studied and other PTMs such as methylation, acetylation, SUMOylation, ADP-ribosylation and glutamylation are being increasingly implicated in antiviral innate immunity. Here we summarize our recent understanding of the most important PTMs regulating the antiviral innate immune response, and their role in virus-related immune pathogenesis.
[Mh] Termos MeSH primário: DNA Viral/imunologia
Imunidade Inata
Processamento de Proteína Pós-Traducional
RNA Viral/imunologia
Viroses/imunologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Interferon Tipo I/genética
Interferon Tipo I/metabolismo
NF-kappa B/metabolismo
Receptores de Reconhecimento de Padrão/metabolismo
Transdução de Sinais
Receptores Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Viral); 0 (Interferon Type I); 0 (NF-kappa B); 0 (RNA, Viral); 0 (Receptors, Pattern Recognition); 0 (Toll-Like Receptors)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171202
[Lr] Data última revisão:
171202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201746959


  7 / 1564 MEDLINE  
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[PMID]:29040278
[Au] Autor:Kumar K; Espaillat A; Cava F
[Ad] Endereço:Laboratory for Molecular Infection Medicine Sweden, Department of Molecular Biology, Umeå Centre for Microbial Research, Umeå University, Umeå, Sweden.
[Ti] Título:PG-Metrics: A chemometric-based approach for classifying bacterial peptidoglycan data sets and uncovering their subjacent chemical variability.
[So] Source:PLoS One;12(10):e0186197, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bacteria cells are protected from osmotic and environmental stresses by an exoskeleton-like polymeric structure called peptidoglycan (PG) or murein sacculus. This structure is fundamental for bacteria's viability and thus, the mechanisms underlying cell wall assembly and how it is modulated serve as targets for many of our most successful antibiotics. Therefore, it is now more important than ever to understand the genetics and structural chemistry of the bacterial cell walls in order to find new and effective methods of blocking it for the treatment of disease. In the last decades, liquid chromatography and mass spectrometry have been demonstrated to provide the required resolution and sensitivity to characterize the fine chemical structure of PG. However, the large volume of data sets that can be produced by these instruments today are difficult to handle without a proper data analysis workflow. Here, we present PG-metrics, a chemometric based pipeline that allows fast and easy classification of bacteria according to their muropeptide chromatographic profiles and identification of the subjacent PG chemical variability between e.g. bacterial species, growth conditions and, mutant libraries. The pipeline is successfully validated here using PG samples from different bacterial species and mutants in cell wall proteins. The obtained results clearly demonstrated that PG-metrics pipeline is a valuable bioanalytical tool that can lead us to cell wall classification and biomarker discovery.
[Mh] Termos MeSH primário: Parede Celular/química
Cromatografia Líquida/estatística & dados numéricos
Espectrometria de Massas/estatística & dados numéricos
Peptidoglicano/química
[Mh] Termos MeSH secundário: Algoritmos
Animais
Antibacterianos/química
Antibacterianos/uso terapêutico
Bactérias/efeitos dos fármacos
Parede Celular/efeitos dos fármacos
Cromatografia Líquida/métodos
Espectrometria de Massas/métodos
Viabilidade Microbiana/efeitos dos fármacos
Modelos Teóricos
Pressão Osmótica/efeitos dos fármacos
Peptidoglicano/classificação
Peptidoglicano/isolamento & purificação
Análise de Componente Principal
Receptores de Reconhecimento de Padrão
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Peptidoglycan); 0 (Receptors, Pattern Recognition)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171018
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186197


  8 / 1564 MEDLINE  
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[PMID]:28931061
[Au] Autor:Sun JJ; Lan JF; Zhao XF; Vasta GR; Wang JX
[Ad] Endereço:Shandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Sciences, Shandong University, Jinan, Shandong, China.
[Ti] Título:Binding of a C-type lectin's coiled-coil domain to the Domeless receptor directly activates the JAK/STAT pathway in the shrimp immune response to bacterial infection.
[So] Source:PLoS Pathog;13(9):e1006626, 2017 Sep.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:C-type lectins (CTLs) are characterized by the presence of a C-type carbohydrate recognition domain (CTLD) that by recognizing microbial glycans, is responsible for their roles as pattern recognition receptors in the immune response to bacterial infection. In addition to the CTLD, however, some CTLs display additional domains that can carry out effector functions, such as the collagenous domain of the mannose-binding lectin. While in vertebrates, the mechanisms involved in these effector functions have been characterized in considerable detail, in invertebrates they remain poorly understood. In this study, we identified in the kuruma shrimp (Marsupenaeus japonicus) a structurally novel CTL (MjCC-CL) that in addition to the canonical CTLD, contains a coiled-coil domain (CCD) responsible for the effector functions that are key to the shrimp's antibacterial response mediated by antimicrobial peptides (AMPs). By the use of in vitro and in vivo experimental approaches we elucidated the mechanism by which the recognition of bacterial glycans by the CTLD of MjCC-CL leads to activation of the JAK/STAT pathway via interaction of the CCD with the surface receptor Domeless, and upregulation of AMP expression. Thus, our study of the shrimp MjCC-CL revealed a striking functional difference with vertebrates, in which the JAK/STAT pathway is indirectly activated by cell death and stress signals through cytokines or growth factors. Instead, by cross-linking microbial pathogens with the cell surface receptor Domeless, a lectin directly activates the JAK/STAT pathway, which plays a central role in the shrimp antibacterial immune responses by upregulating expression of selected AMPs.
[Mh] Termos MeSH primário: Proteínas de Artrópodes/metabolismo
Crustáceos/metabolismo
Lectinas Tipo C/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Proteínas de Artrópodes/imunologia
Crustáceos/microbiologia
DNA Complementar/genética
Janus Quinases/metabolismo
Lectinas Tipo C/química
Receptores de Reconhecimento de Padrão/metabolismo
Fatores de Transcrição STAT/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arthropod Proteins); 0 (DNA, Complementary); 0 (Lectins, C-Type); 0 (Receptors, Pattern Recognition); 0 (STAT Transcription Factors); EC 2.7.10.2 (Janus Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006626


  9 / 1564 MEDLINE  
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[PMID]:28801521
[Au] Autor:Wilhelm I; Nyúl-Tóth Á; Kozma M; Farkas AE; Krizbai IA
[Ad] Endereço:Institute of Biophysics, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary; and wilhelm.imola@brc.mta.hu.
[Ti] Título:Role of pattern recognition receptors of the neurovascular unit in inflamm-aging.
[So] Source:Am J Physiol Heart Circ Physiol;313(5):H1000-H1012, 2017 Nov 01.
[Is] ISSN:1522-1539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aging is associated with chronic inflammation partly mediated by increased levels of damage-associated molecular patterns, which activate pattern recognition receptors (PRRs) of the innate immune system. Furthermore, many aging-related disorders are associated with inflammation. PRRs, such as Toll-like receptors (TLRs) and nucleotide-binding oligomerization domain-like receptors (NLRs), are expressed not only in cells of the innate immune system but also in other cells, including cells of the neurovascular unit and cerebral vasculature forming the blood-brain barrier. In this review, we summarize our present knowledge about the relationship between activation of PRRs expressed by cells of the neurovascular unit-blood-brain barrier, chronic inflammation, and aging-related pathologies of the brain. The most important damage-associated molecular pattern-sensing PRRs in the brain are TLR2, TLR4, and NLR family pyrin domain-containing protein-1 and pyrin domain-containing protein-3, which are activated during physiological and pathological aging in microglia, neurons, astrocytes, and possibly endothelial cells and pericytes.
[Mh] Termos MeSH primário: Envelhecimento/metabolismo
Barreira Hematoencefálica/metabolismo
Inflamassomos/metabolismo
Inflamação/metabolismo
Microvasos/metabolismo
Acoplamento Neurovascular
Receptores de Reconhecimento de Padrão/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Fatores Etários
Envelhecimento/imunologia
Animais
Barreira Hematoencefálica/imunologia
Barreira Hematoencefálica/fisiopatologia
Seres Humanos
Imunidade Inata
Inflamassomos/imunologia
Inflamação/imunologia
Inflamação/fisiopatologia
Microvasos/imunologia
Microvasos/fisiopatologia
Proteínas NLR/imunologia
Proteínas NLR/metabolismo
Receptores de Reconhecimento de Padrão/imunologia
Receptor 2 Toll-Like/imunologia
Receptor 2 Toll-Like/metabolismo
Receptor 4 Toll-Like/imunologia
Receptor 4 Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Inflammasomes); 0 (NLR Proteins); 0 (Receptors, Pattern Recognition); 0 (Toll-Like Receptor 2); 0 (Toll-Like Receptor 4)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170813
[St] Status:MEDLINE
[do] DOI:10.1152/ajpheart.00106.2017


  10 / 1564 MEDLINE  
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[PMID]:28794024
[Au] Autor:Huang C; Kolokoltsova OA; Mateer EJ; Koma T; Paessler S
[Ad] Endereço:Department of Pathology and Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, Texas, USA chhuang@utmb.edu slpaessl@utmb.edu.
[Ti] Título:Highly Pathogenic New World Arenavirus Infection Activates the Pattern Recognition Receptor Protein Kinase R without Attenuating Virus Replication in Human Cells.
[So] Source:J Virol;91(20), 2017 Oct 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The arenavirus family consists of several highly pathogenic viruses, including the Old World (OW) arenavirus Lassa fever virus (LASV) and the New World (NW) Junin virus (JUNV) and Machupo virus (MACV). Host response to infection by these pathogenic arenaviruses is distinct in many aspects. JUNV and MACV infections readily induce an interferon (IFN) response in human cells, while LASV infection usually triggers an undetectable or weak IFN response. JUNV induces an IFN response through RIG-I, suggesting that the host non-self RNA sensor readily detects JUNV viral RNAs (vRNAs) during infection and activates IFN response. Double-stranded-RNA (dsRNA)-activated protein kinase R (PKR) is another host non-self RNA sensor classically known for its vRNA recognition activity. Here we report that infection with NW arenaviruses JUNV and MACV, but not OW LASV, activated PKR, concomitant with elevated phosphorylation of the translation initiation factor α subunit of eukaryotic initiation factor 2 (eIF2α). Host protein synthesis was substantially suppressed in MACV- and JUNV-infected cells but was only marginally reduced in LASV-infected cells. Despite the antiviral activity known for PKR against many other viruses, the replication of JUNV and MACV was not impaired but was slightly augmented in wild-type (wt) cells compared to that in PKR-deficient cells, suggesting that PKR or PKR activation did not negatively affect JUNV and MACV infection. Additionally, we found an enhanced IFN response in JUNV- or MACV-infected PKR-deficient cells, which was inversely correlated with virus replication. The detection of viral RNA by host non-self RNA sensors, including RIG-I and MDA5, is critical to the initiation of the innate immune response to RNA virus infection. Among pathogenic arenaviruses, the OW LASV usually does not elicit an interferon response. However, the NW arenaviruses JUNV and MACV readily trigger an IFN response in a RIG-I-dependent manner. Here, we demonstrate for the first time that pathogenic NW arenaviruses JUNV and MACV, but not the OW arenavirus LASV, activated the dsRNA-dependent PKR, another host non-self RNA sensor, during infection. Interestingly, the replication of JUNV and MACV was not restricted but was rather slightly augmented in the presence of PKR. Our data provide new evidence for a distinct interplay between host non-self RNA sensors and pathogenic arenaviruses, which also provides insights into the pathogenesis of arenaviruses and may facilitate the design of vaccines and treatments against arenavirus-caused diseases.
[Mh] Termos MeSH primário: Arenavirus do Novo Mundo/patogenicidade
Arenavirus do Velho Mundo/patogenicidade
Imunidade Inata
Vírus Junin/patogenicidade
Receptores de Reconhecimento de Padrão/metabolismo
Replicação Viral
eIF-2 Quinase/metabolismo
[Mh] Termos MeSH secundário: Células A549
Arenavirus do Novo Mundo/fisiologia
Arenavirus do Velho Mundo/fisiologia
Interações Hospedeiro-Patógeno
Seres Humanos
Interferons/biossíntese
Interferons/imunologia
Vírus Junin/fisiologia
Fosforilação
Receptores de Reconhecimento de Padrão/genética
Fatores de Transcrição/metabolismo
eIF-2 Quinase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Pattern Recognition); 0 (Transcription Factors); 181233-60-3 (ELF2 protein, human); 9008-11-1 (Interferons); EC 2.7.11.1 (EIF2AK2 protein, human); EC 2.7.11.1 (eIF-2 Kinase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE



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