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[PMID]:28901890
[Au] Autor:Zhang B; Lv Z; Li H; Guo S; Liu D; Guo Y
[Ad] Endereço:State Key Laboratory of Animal Nutrition,College of Animal Science and Technology,China Agricultural University,Beijing 100193,People's Republic of China.
[Ti] Título:Dietary l-arginine inhibits intestinal Clostridium perfringens colonisation and attenuates intestinal mucosal injury in broiler chickens.
[So] Source:Br J Nutr;118(5):321-332, 2017 Sep.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We investigated the effects of dietary l-arginine level and feeding duration on the intestinal damage of broilers induced by Clostridium perfringens (CP) in vivo, and the antimicrobial effect of its metabolite nitric oxide (NO) in vitro. The in vivo experiment was designed as a factorial arrangement of three dietary treatments×two challenge statuses. Broilers were fed a basal diet (CON) or a high-arginine diet (ARG) containing 1·87 % l-arginine, or CON for the first 8 d and ARG from days 9 to 28 (CON/ARG). Birds were co-infected with or without Eimeria and CP (EM/CP). EM/CP challenge led to intestinal injury, as evidenced by lower plasma d-xylose concentration (P<0·01), higher paracellular permeability in the ileum (P<0·05) and higher numbers of Escherichia coli (P<0·05) and CP (P<0·001) in caecal digesta; however, this situation could be alleviated by l-arginine supplementation (P<0·05). The intestinal claudin-1 and occludin mRNA expression levels were decreased (P<0·05) following EM/CP challenge; this was reversed by l-arginine supplementation (P<0·05). Moreover, EM/CP challenge up-regulated (P<0·05) claudin-2, interferon-γ (IFN-γ), toll-like receptor 2 and nucleotide-binding oligomerisation domain 1 (NOD1) mRNA expression, and l-arginine supplementation elevated (P<0·05) IFN-γ, IL-10 and NOD1 mRNA expression. In vitro study showed that NO had bacteriostatic activity against CP (P<0·001). In conclusion, l-arginine supplementation could inhibit CP overgrowth and alleviate intestinal mucosal injury by modulating innate immune responses, enhancing barrier function and producing NO.
[Mh] Termos MeSH primário: Arginina/administração & dosagem
Clostridium perfringens/efeitos dos fármacos
Dieta/veterinária
Imunidade Inata
Mucosa Intestinal/efeitos dos fármacos
Intestinos/microbiologia
[Mh] Termos MeSH secundário: Ração Animal/análise
Animais
Galinhas
Claudina-1/genética
Claudina-1/metabolismo
Claudina-2/genética
Claudina-2/metabolismo
Suplementos Nutricionais
Eimeria/efeitos dos fármacos
Escherichia coli/efeitos dos fármacos
Microbioma Gastrointestinal/efeitos dos fármacos
Interferon gama/genética
Interferon gama/metabolismo
Interleucina-10/genética
Interleucina-10/metabolismo
Mucosa Intestinal/metabolismo
Intestinos/efeitos dos fármacos
Óxido Nítrico/metabolismo
Proteína Adaptadora de Sinalização NOD1/genética
Proteína Adaptadora de Sinalização NOD1/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptor 2 Toll-Like/genética
Receptor 2 Toll-Like/metabolismo
Regulação para Cima
Xilose/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Claudin-1); 0 (Claudin-2); 0 (Nod1 Signaling Adaptor Protein); 0 (RNA, Messenger); 0 (Toll-Like Receptor 2); 130068-27-8 (Interleukin-10); 31C4KY9ESH (Nitric Oxide); 82115-62-6 (Interferon-gamma); 94ZLA3W45F (Arginine); A1TA934AKO (Xylose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170914
[St] Status:MEDLINE
[do] DOI:10.1017/S0007114517002094


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[PMID]:28878001
[Au] Autor:Hayakawa K; Formica AM; Zhou Y; Ichikawa D; Asano M; Li YS; Shinton SA; Brill-Dashoff J; Núñez G; Hardy RR
[Ad] Endereço:Fox Chase Cancer Center, Philadelphia, PA kyoko.hayakawa@fccc.edu.
[Ti] Título:NLR Nod1 signaling promotes survival of BCR-engaged mature B cells through up-regulated Nod1 as a positive outcome.
[So] Source:J Exp Med;214(10):3067-3083, 2017 Oct 02.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although B cell development requires expression of the B cell antigen receptor (BCR), it remains unclear whether engagement of self-antigen provides a positive impact for most B cells. Here, we show that BCR engagement by self-ligand during development in vivo results in up-regulation of the Nod-like receptor member Nod1, which recognizes the products of intestinal commensal bacteria. In anti-thymocyte/Thy-1 autoreactive BCR knock-in mice lacking self-Thy-1 ligand, immunoglobulin light chain editing occurred, generating B cells with up-regulated Nod1, including follicular and marginal zone B cells with natural autoreactivity. This BCR editing with increased Nod1 resulted in preferential survival. In normal adult mice, most mature B cells are enriched for Nod1 up-regulated cells, and signaling through Nod1 promotes competitive survival of mature B cells. These findings demonstrate a role for microbial products in promoting survival of mature B cells through up-regulated Nod1, providing a positive effect of BCR engagement on development of most B cells.
[Mh] Termos MeSH primário: Linfócitos B/fisiologia
Proteínas NLR/fisiologia
Proteína Adaptadora de Sinalização NOD1/fisiologia
Receptores de Antígenos de Linfócitos B/fisiologia
[Mh] Termos MeSH secundário: Envelhecimento/fisiologia
Animais
Linfócitos B/metabolismo
Técnicas de Introdução de Genes
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Transdução de Sinais/fisiologia
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Card4 protein, mouse); 0 (NLR Proteins); 0 (Nod1 Signaling Adaptor Protein); 0 (Receptors, Antigen, B-Cell)
[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:170908
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20170497


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[PMID]:28673961
[Au] Autor:Vijayrajratnam S; Pushkaran AC; Balakrishnan A; Vasudevan AK; Biswas R; Mohan CG
[Ad] Endereço:Center for Nanosciences and Molecular Medicine, Amrita University, Kochi, Kerala 682041, India.
[Ti] Título:Understanding the molecular differential recognition of muramyl peptide ligands by LRR domains of human NOD receptors.
[So] Source:Biochem J;474(16):2691-2711, 2017 Jul 27.
[Is] ISSN:1470-8728
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Human nucleotide-binding oligomerization domain proteins, hNOD1 and hNOD2, are host intracellular receptors with C-terminal leucine-rich repeat (LRR) domains, which recognize specific bacterial peptidoglycan (PG) fragments as their ligands. The specificity of this recognition is dependent on the third amino acid of the stem peptide of the PG ligand, which is usually -diaminopimelic acid ( DAP) or l-lysine (l-Lys). Since the LRR domains of hNOD receptors had been experimentally shown to confer the PG ligand-sensing specificity, we developed three-dimensional structures of hNOD1-LRR and the hNOD2-LRR to understand the mechanism of differential recognition of muramyl peptide ligands by hNOD receptors. The hNOD1-LRR and hNOD2-LRR receptor models exhibited right-handed curved solenoid shape. The hot-spot residues experimentally proved to be critical for ligand recognition were located in the concavity of the NOD-LRR and formed the recognition site. Our molecular docking analyses and molecular electrostatic potential mapping studies explain the activation of hNOD-LRRs, in response to effective molecular interactions of PG ligands at the recognition site; and conversely, the inability of certain PG ligands to activate hNOD-LRRs, by deviations from the recognition site. Based on molecular docking studies using PG ligands, we propose few residues - G825, D826 and N850 in hNOD1-LRR and L904, G905, W931, L932 and S933 in hNOD2-LRR, evolutionarily conserved across different host species, which may play a major role in ligand recognition. Thus, our integrated experimental and computational approach elucidates the molecular basis underlying the differential recognition of PG ligands by hNOD receptors.
[Mh] Termos MeSH primário: Acetilmuramil-Alanil-Isoglutamina/química
Simulação de Acoplamento Molecular
Proteína Adaptadora de Sinalização NOD1/química
Proteína Adaptadora de Sinalização NOD2/química
[Mh] Termos MeSH secundário: Acetilmuramil-Alanil-Isoglutamina/genética
Acetilmuramil-Alanil-Isoglutamina/metabolismo
Células HEK293
Seres Humanos
Ligantes
Proteína Adaptadora de Sinalização NOD1/genética
Proteína Adaptadora de Sinalização NOD1/metabolismo
Proteína Adaptadora de Sinalização NOD2/genética
Proteína Adaptadora de Sinalização NOD2/metabolismo
Domínios Proteicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ligands); 0 (NOD1 protein, human); 0 (NOD2 protein, human); 0 (Nod1 Signaling Adaptor Protein); 0 (Nod2 Signaling Adaptor Protein); 53678-77-6 (Acetylmuramyl-Alanyl-Isoglutamine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170803
[Lr] Data última revisão:
170803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE
[do] DOI:10.1042/BCJ20170220


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[PMID]:28652394
[Au] Autor:Kasimsetty SG; Shigeoka AA; Scheinok AA; Gavin AL; Ulevitch RJ; McKay DB
[Ad] Endereço:Division of Nephrology and Hypertension, Department of Medicine, University of California, San Diego, La Jolla, CA 92093; and.
[Ti] Título:Lack of Both Nucleotide-Binding Oligomerization Domain-Containing Proteins 1 and 2 Primes T Cells for Activation-Induced Cell Death.
[So] Source:J Immunol;199(3):1196-1205, 2017 Aug 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nucleotide-binding oligomerization domain (Nod)-containing proteins Nod1 and Nod2 play important roles in the innate immune response to pathogenic microbes, but mounting data suggest these pattern recognition receptors might also play key roles in adaptive immune responses. Targeting Nod1 and Nod2 signaling pathways in T cells is likely to provide a new strategy to modify inflammation in a variety of disease states, particularly those that depend on Ag-induced T cell activation. To better understand how Nod1 and Nod2 proteins contribute to adaptive immunity, this study investigated their role in alloantigen-induced T cell activation and asked whether their absence might impact in vivo alloresponses using a severe acute graft versus host disease model. The study provided several important observations. We found that the simultaneous absence of Nod1 and Nod2 primed T cells for activation-induced cell death. T cells from mice rapidly underwent cell death upon exposure to alloantigen. The T cells had sustained p53 expression that was associated with downregulation of its negative regulator MDM2. In vivo, mice transplanted with an inoculum containing T cells were protected from severe graft versus host disease. The results show that the simultaneous absence of Nod1 and Nod2 is associated with accelerated T cell death upon alloantigen encounter, suggesting these proteins might provide new targets to ameliorate T cell responses in a variety of inflammatory states, including those associated with bone marrow or solid organ transplantation.
[Mh] Termos MeSH primário: Ativação Linfocitária
Proteína Adaptadora de Sinalização NOD1/metabolismo
Proteína Adaptadora de Sinalização NOD2/metabolismo
Linfócitos T/imunologia
Linfócitos T/fisiologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Animais
Morte Celular
Modelos Animais de Doenças
Regulação para Baixo
Genes p53/genética
Genes p53/imunologia
Doença Enxerto-Hospedeiro/imunologia
Imunidade Inata
Isoantígenos/imunologia
Camundongos
Proteína Adaptadora de Sinalização NOD1/deficiência
Proteína Adaptadora de Sinalização NOD1/genética
Proteína Adaptadora de Sinalização NOD2/deficiência
Proteína Adaptadora de Sinalização NOD2/genética
Proteínas Proto-Oncogênicas c-mdm2/genética
Proteínas Proto-Oncogênicas c-mdm2/imunologia
Proteínas Proto-Oncogênicas c-mdm2/metabolismo
Receptores de Reconhecimento de Padrão/imunologia
Receptores de Reconhecimento de Padrão/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Card4 protein, mouse); 0 (Isoantigens); 0 (Nod1 Signaling Adaptor Protein); 0 (Nod2 Signaling Adaptor Protein); 0 (Receptors, Pattern Recognition); EC 2.3.2.27 (Mdm2 protein, mouse); EC 2.3.2.27 (Proto-Oncogene Proteins c-mdm2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600667


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[PMID]:28576260
[Au] Autor:Ohlsson C; Nigro G; Boneca IG; Bäckhed F; Sansonetti P; Sjögren K
[Ad] Endereço:Centre for Bone and Arthritis Research, Institute of Medicin, Sahlgrenska Academy at University of Gothenburg, SE-413 45 Gothenburg, Sweden.
[Ti] Título:Regulation of bone mass by the gut microbiota is dependent on NOD1 and NOD2 signaling.
[So] Source:Cell Immunol;317:55-58, 2017 Jul.
[Is] ISSN:1090-2163
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Germ-free (GF) mice have increased bone mass that is normalized by colonization with gut microbiota (GM) from conventionally raised (CONV-R) mice. To determine if innate immune signaling pathways mediated the effect of the GM, we studied the skeleton of GF and CONV-R mice with targeted inactivation of MYD88, NOD1 or NOD2. In contrast to WT and Myd88 mice, cortical bone thickness in mice lacking Nod1 or Nod2 was not increased under GF conditions. The expression of Tnfα and the osteoclastogenic factor Rankl in bone was reduced in GF compared to CONV-R WT mice but not in Nod1 or Nod2 mice indicating that the effect of the GM to increase Tnfα and Rankl in bone and to reduce bone mass is dependent on both NOD1 and NOD2 signaling.
[Mh] Termos MeSH primário: Osso e Ossos/imunologia
Microbioma Gastrointestinal/imunologia
Proteína Adaptadora de Sinalização NOD1/metabolismo
Proteína Adaptadora de Sinalização NOD2/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Desenvolvimento Ósseo/imunologia
Células Cultivadas
Feminino
Vida Livre de Germes
Imunidade Inata
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fator 88 de Diferenciação Mieloide/genética
Fator 88 de Diferenciação Mieloide/metabolismo
Proteína Adaptadora de Sinalização NOD1/genética
Proteína Adaptadora de Sinalização NOD2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Card15 protein, mouse); 0 (Card4 protein, mouse); 0 (Myd88 protein, mouse); 0 (Myeloid Differentiation Factor 88); 0 (Nod1 Signaling Adaptor Protein); 0 (Nod2 Signaling Adaptor Protein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170604
[St] Status:MEDLINE


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[PMID]:28541685
[Au] Autor:Wang S; Yang J; Li X; Liu Z; Wu Y; Si G; Tao Y; Zhao N; Hu X; Ma Y; Liu G
[Ad] Endereço:Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College , 2A Nanwei Road, Xicheng District, Beijing 100050, P. R. China.
[Ti] Título:Discovery of 1,4-Benzodiazepine-2,5-dione (BZD) Derivatives as Dual Nucleotide Binding Oligomerization Domain Containing 1/2 (NOD1/NOD2) Antagonists Sensitizing Paclitaxel (PTX) To Suppress Lewis Lung Carcinoma (LLC) Growth in Vivo.
[So] Source:J Med Chem;60(12):5162-5192, 2017 Jun 22.
[Is] ISSN:1520-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nucleotide-binding oligomerization domain-like receptors (NLRs) are intracellular sensors of pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). Previously, we reported nucleotide-binding oligomerization domain-containing protein 1 (NOD1) antagonists (11, 12) and a NOD2 antagonist (9) that sensitized docetaxel (DTX) or paclitaxel (PTX) treatment for breast or lung cancer. In this article, we describe for the first time a 1,4-benzodiazepine-2,5-dione (BZD) derivative (26bh) that acts as a dual NOD1/NOD2 antagonist and inhibits both nuclear factor κB (NF-κB) and mitogen-activated protein kinase (MAPK) inflammatory signaling, thereby sensitizing PTX to suppress Lewis lung carcinoma (LLC) growth. After investigation of the compound's cytotoxicity, a systematic structure-activity relationship (SAR) was completed and revealed several key factors that were necessary to maintain antagonistic ability. This study establishes the possibility for using adjuvant treatment to combat cancer by antagonizing both NOD1 and NOD2 signaling.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Benzodiazepinas/química
Carcinoma Pulmonar de Lewis/tratamento farmacológico
Proteína Adaptadora de Sinalização NOD1/antagonistas & inibidores
Proteína Adaptadora de Sinalização NOD2/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Benzodiazepinas/farmacologia
Citocinas/metabolismo
Ensaios de Seleção de Medicamentos Antitumorais/métodos
Seres Humanos
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Terapia de Alvo Molecular
Paclitaxel/administração & dosagem
Domínios Proteicos
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (NOD1 protein, human); 0 (NOD2 protein, human); 0 (Nod1 Signaling Adaptor Protein); 0 (Nod2 Signaling Adaptor Protein); 12794-10-4 (Benzodiazepines); P88XT4IS4D (Paclitaxel)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170811
[Lr] Data última revisão:
170811
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jmedchem.7b00608


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[PMID]:28300841
[Au] Autor:Sahu U; Choudhury A; Parvez S; Biswas S; Kar S
[Ad] Endereço:Jamia Hamdard-Institute of Molecular Medicine, Jamia Hamdard, New Delhi 110062, India.
[Ti] Título:Induction of intestinal stemness and tumorigenicity by aberrant internalization of commensal non-pathogenic E. coli.
[So] Source:Cell Death Dis;8(3):e2667, 2017 Mar 16.
[Is] ISSN:2041-4889
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Commensal Escherichia coli has been identified as a major protagonist of microbe-induced colorectal oncogenesis. Its tumour-promoting attribute is linked to the expression of DNA-damaging genotoxins. Using a constitutively invasive variant of non-pathogenic E. coli, we demonstrate that chronic presence of internalized E. coli leads to enhanced oncogenicity in colon cancer cells. Instead of genomic damage, the tumorigenic effect is mediated through an expansion of the cancer stem cell (CSC) population, likely through dedifferentiation of lineage-committed intestinal epithelial cells. Stemness-linked intestinal tumorigenicity is directly correlated to absence of microbial virulence factor expression and is specific for intestinal cells. The enriched CSC fraction remains stable in the absence of the instigating bacteria and can foster stemness traits in unexposed cells through secreted factors. Mechanistically, aberrant host invasion leads to realignment of multiple host signal transduction cascades, notably mutually re-enforcing NF-κB and ß-catenin activation, through reciprocal modulation of microbe sensing pathways Nod1/Rip2 and TLR/MyD88. The expanded tumorigenic CSC population is marked by enhanced malignancy traits, long-term self-renewal capacity and robust tumorigenic ability, both in vitro and in vivo. Our study shows that microbe-induced oncogenicity is not a strict correlate of commensal virulence and can be invoked by even non-pathogenic E. coli by engendering tumorigenic stemness in host cells.
[Mh] Termos MeSH primário: Carcinogênese/metabolismo
Escherichia coli/patogenicidade
Intestinos/microbiologia
Intestinos/patologia
Células-Tronco Neoplásicas/microbiologia
Células-Tronco Neoplásicas/patologia
[Mh] Termos MeSH secundário: Animais
Células CACO-2
Carcinogênese/patologia
Linhagem Celular Tumoral
Colo/metabolismo
Colo/microbiologia
Colo/patologia
Células Epiteliais/metabolismo
Células Epiteliais/microbiologia
Células Epiteliais/patologia
Células HCT116
Células HT29
Células Hep G2
Seres Humanos
Intestinos/metabolismo
Masculino
Camundongos
Camundongos Nus
Fator 88 de Diferenciação Mieloide/metabolismo
NF-kappa B/metabolismo
Células-Tronco Neoplásicas/metabolismo
Proteína Adaptadora de Sinalização NOD1/metabolismo
Proteína Serina-Treonina Quinase 2 de Interação com Receptor/metabolismo
Transdução de Sinais/fisiologia
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Myeloid Differentiation Factor 88); 0 (NF-kappa B); 0 (Nod1 Signaling Adaptor Protein); 0 (beta Catenin); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinase 2)
[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:170317
[St] Status:MEDLINE
[do] DOI:10.1038/cddis.2017.27


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[PMID]:28240593
[Au] Autor:Kim HW; Kwon YJ; Park BW; Song JJ; Park YB; Park MC
[Ad] Endereço:Division of Rheumatology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, South Korea.
[Ti] Título:Differential expressions of NOD-like receptors and their associations with inflammatory responses in rheumatoid arthritis.
[So] Source:Clin Exp Rheumatol;35(4):630-637, 2017 Jul-Aug.
[Is] ISSN:0392-856X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To determine the differential expressions of nucleotide oligomerisation domain (NOD)-like receptors (NLRs) and to investigate their association with inflammatory responses in rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS). METHODS: Gene expression and protein levels of various NLRs, including NOD1, NOD2, NLRP1, NLRP3, NLRP12, NLRX1, and NLRC3, were determined in FLS and synovial tissues from patients with RA and patients with osteoarthritis (OA) using quantitative real-time PCR and immunohistochemistry. After transfection of NOD2 RNAi plasmids or a pcDNA3.1-NLRX1 vector, gene expression levels of pro-inflammatory cytokines in RA FLS and the protein levels of these cytokines in culture supernatants were determined using quantitative real-time PCR and enzyme-linked immunosorbent assays. The effects of NLR gene regulation on NF-κB and caspase-1 were evaluated using Western blot analysis. RESULTS: Gene expression levels of NOD1, NLRP1, NLRP3, NLRP12, and NLRC3 were not different between RA and OA samples. NOD2 gene expression and protein levels were significantly increased in RA samples, whereas the levels of NLRX1 were significantly decreased. Downregulation of NOD2 gene expression by transfection with NOD2 RNAi plasmid significantly reduced pro-inflammatory cytokine levels in RA FLS, while transfection with adenoviral vectors encoding NLRX1 had no effect on pro-inflammatory cytokine levels. Downregulation of NOD2 gene expression significantly decreased NF-κB, TRAF6, and IKK levels, but not caspase-1 levels, in RA FLS. CONCLUSIONS: NOD2 is upregulated in RA FLS; moreover, downregulation of NOD2 gene expression reduces pro-inflammatory cytokine and NF-κB levels in RA FLS. These findings provide evidence that NOD2 exerts pro-inflammatory effects in RA.
[Mh] Termos MeSH primário: Artrite Reumatoide/genética
Membrana Sinovial/metabolismo
Sinoviócitos/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Proteínas Reguladoras de Apoptose/genética
Proteínas Reguladoras de Apoptose/metabolismo
Artrite Reumatoide/metabolismo
Artrite Reumatoide/cirurgia
Artroplastia do Joelho
Western Blotting
Estudos de Casos e Controles
Caspase 1/metabolismo
Regulação para Baixo
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Quinase I-kappa B/metabolismo
Imuno-Histoquímica
Peptídeos e Proteínas de Sinalização Intercelular/genética
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Peptídeos e Proteínas de Sinalização Intracelular/genética
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Proteínas Mitocondriais/genética
Proteínas Mitocondriais/metabolismo
NF-kappa B/metabolismo
Proteína 3 que Contém Domínio de Pirina da Família NLR/genética
Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo
Proteína Adaptadora de Sinalização NOD1/genética
Proteína Adaptadora de Sinalização NOD1/metabolismo
Proteína Adaptadora de Sinalização NOD2/genética
Proteína Adaptadora de Sinalização NOD2/metabolismo
Osteoartrite do Joelho/genética
Osteoartrite do Joelho/metabolismo
Osteoartrite do Joelho/cirurgia
Interferência de RNA
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Fator 6 Associado a Receptor de TNF/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Apoptosis Regulatory Proteins); 0 (Intercellular Signaling Peptides and Proteins); 0 (Intracellular Signaling Peptides and Proteins); 0 (Mitochondrial Proteins); 0 (NF-kappa B); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (NLRC3 protein, human); 0 (NLRP1 protein, human); 0 (NLRP12 protein, human); 0 (NLRP3 protein, human); 0 (NLRX1 protein, human); 0 (NOD1 protein, human); 0 (NOD2 protein, human); 0 (Nod1 Signaling Adaptor Protein); 0 (Nod2 Signaling Adaptor Protein); 0 (RNA, Messenger); 0 (TNF Receptor-Associated Factor 6); 0 (Tifab protein, human); EC 2.7.11.10 (I-kappa B Kinase); EC 3.4.22.36 (Caspase 1)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170831
[Lr] Data última revisão:
170831
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170228
[St] Status:MEDLINE


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[PMID]:28202617
[Au] Autor:Martinic MM; Caminschi I; O'Keeffe M; Thinnes TC; Grumont R; Gerondakis S; McKay DB; Nemazee D; Gavin AL
[Ad] Endereço:Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037.
[Ti] Título:The Bacterial Peptidoglycan-Sensing Molecules NOD1 and NOD2 Promote CD8 Thymocyte Selection.
[So] Source:J Immunol;198(7):2649-2660, 2017 Apr 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nucleotide-binding and oligomerization domain (NOD)-like receptors NOD1 and NOD2 are cytosolic innate immune receptors that recognize microbial peptidoglycans. Although studies have addressed the role of NOD proteins in innate immune responses, little attention has been given to their impact on the developing adaptive immune system. We have assessed the roles of NOD1 and NOD2 deficiency on T cell development in mice. Our results demonstrate that NOD1 and NOD2 promote the positive selection/maturation of CD8 single-positive thymocytes in a thymocyte-intrinsic manner. TCR-mediated ERK phosphorylation is significantly reduced in the absence of NOD proteins, but receptor-interacting protein 2 is not involved in CD8 single-positive thymocyte selection or ERK signaling. Commensal bacteria-free animals have thymocyte maturation defects, and exogenous NOD ligands can enhance thymocyte maturation in culture. These results raise the intriguing possibility that abnormal lymphocyte responses observed in NOD-dependent inflammatory diseases are not driven solely by microbial signals in the gut, but may also involve intrinsic lymphocyte defects resulting from impaired CD8 T cell thymic development.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/citologia
Diferenciação Celular/imunologia
Proteína Adaptadora de Sinalização NOD1/imunologia
Proteína Adaptadora de Sinalização NOD2/imunologia
Timócitos/citologia
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD8-Positivos/imunologia
Immunoblotting
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Reação em Cadeia da Polimerase
Timócitos/imunologia
Timo/citologia
Timo/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Card15 protein, mouse); 0 (Card4 protein, mouse); 0 (Nod1 Signaling Adaptor Protein); 0 (Nod2 Signaling Adaptor Protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170815
[Lr] Data última revisão:
170815
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170217
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601462


  10 / 578 MEDLINE  
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[PMID]:28157451
[Au] Autor:Wiese KM; Coates BM; Ridge KM
[Ad] Endereço:Departments of 1 Medicine and.
[Ti] Título:The Role of Nucleotide-Binding Oligomerization Domain-Like Receptors in Pulmonary Infection.
[So] Source:Am J Respir Cell Mol Biol;57(2):151-161, 2017 Aug.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pneumonia is caused by both viral and bacterial pathogens and is responsible for a significant health burden in the Unites States. The innate immune system is the human body's first line of defense against these pathogens. The recognition of invading pathogens via pattern recognition receptors leads to proinflammatory cytokine and chemokine production, followed by recruitment and activation of effector immune cells. The nonspecific inflammatory nature of the innate immune response can result in immunopathology that is detrimental to the host. In this review, we focus on one class of pattern recognition receptors, the nucleotide-binding oligomerization domain (NOD)-like receptors, specifically NOD1 and NOD2, and their role in host defense against viral and bacterial pathogens of the lung, including influenza, respiratory syncytial virus, Streptococcus pneumoniae, Chlamydophila pneumoniae, and Staphylococcus aureus. It is hoped that improved understanding of NOD1 and NOD2 activity in pneumonia will facilitate the development of novel therapies and promote improved patient outcomes.
[Mh] Termos MeSH primário: Imunidade Inata
Proteína Adaptadora de Sinalização NOD1/imunologia
Proteína Adaptadora de Sinalização NOD2/imunologia
Pneumonia Bacteriana/imunologia
Pneumonia Viral/imunologia
Receptores de Reconhecimento de Padrão/imunologia
[Mh] Termos MeSH secundário: Acetilmuramil-Alanil-Isoglutamina/imunologia
Imunidade Adaptativa
Células Epiteliais Alveolares/imunologia
Animais
Seres Humanos
Fator Regulador 3 de Interferon/imunologia
Leucina
Camundongos
NF-kappa B/fisiologia
Domínios Proteicos
Sequências Repetitivas de Aminoácidos
Transdução de Sinais/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (IRF3 protein, human); 0 (Interferon Regulatory Factor-3); 0 (NF-kappa B); 0 (NOD1 protein, human); 0 (NOD2 protein, human); 0 (Nod1 Signaling Adaptor Protein); 0 (Nod2 Signaling Adaptor Protein); 0 (Receptors, Pattern Recognition); 53678-77-6 (Acetylmuramyl-Alanyl-Isoglutamine); GMW67QNF9C (Leucine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170917
[Lr] Data última revisão:
170917
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170204
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2016-0375TR



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