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[PMID]:28860194
[Au] Autor:Scott NE; Giogha C; Pollock GL; Kennedy CL; Webb AI; Williamson NA; Pearson JS; Hartland EL
[Ad] Endereço:From the Department of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Melbourne 3000, Australia, nichollas.scott@unimelb.edu.au.
[Ti] Título:The bacterial arginine glycosyltransferase effector NleB preferentially modifies Fas-associated death domain protein (FADD).
[So] Source:J Biol Chem;292(42):17337-17350, 2017 Oct 20.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The inhibition of host innate immunity pathways is essential for the persistence of attaching and effacing pathogens such as enteropathogenic (EPEC) and during mammalian infections. To subvert these pathways and suppress the antimicrobial response, attaching and effacing pathogens use type III secretion systems to introduce effectors targeting key signaling pathways in host cells. One such effector is the arginine glycosyltransferase NleB1 (NleB in ) that modifies conserved arginine residues in death domain-containing host proteins with -acetylglucosamine (GlcNAc), thereby blocking extrinsic apoptosis signaling. Ectopically expressed NleB1 modifies the host proteins Fas-associated via death domain (FADD), TNFRSF1A-associated via death domain (TRADD), and receptor-interacting serine/threonine protein kinase 1 (RIPK1). However, the full repertoire of arginine GlcNAcylation induced by pathogen-delivered NleB1 is unknown. Using an affinity proteomic approach for measuring arginine-GlcNAcylated glycopeptides, we assessed the global profile of arginine GlcNAcylation during ectopic expression of NleB1, EPEC infection , or infection NleB overexpression resulted in arginine GlcNAcylation of multiple host proteins. However, NleB delivery during EPEC and infection caused rapid and preferential modification of Arg in FADD. This FADD modification was extremely stable and insensitive to physiological temperatures, glycosidases, or host cell degradation. Despite its stability and effect on the inhibition of apoptosis, arginine GlcNAcylation did not elicit any proteomic changes, even in response to prolonged NleB1 expression. We conclude that, at normal levels of expression during bacterial infection, NleB1/NleB antagonizes death receptor-induced apoptosis of infected cells by modifying FADD in an irreversible manner.
[Mh] Termos MeSH primário: Apoptose
Citrobacter rodentium/enzimologia
Escherichia coli Enteropatogênica/enzimologia
Infecções por Escherichia coli/metabolismo
Proteínas de Escherichia coli/metabolismo
Proteína de Domínio de Morte Associada a Fas/metabolismo
Glicosiltransferases/metabolismo
Processamento de Proteína Pós-Traducional
Fatores de Virulência/metabolismo
[Mh] Termos MeSH secundário: Citrobacter rodentium/patogenicidade
Escherichia coli Enteropatogênica/patogenicidade
Infecções por Escherichia coli/genética
Infecções por Escherichia coli/patologia
Proteínas de Escherichia coli/genética
Proteína de Domínio de Morte Associada a Fas/genética
Glicosiltransferases/genética
Células HeLa
Seres Humanos
Estabilidade Proteica
Proteína Serina-Treonina Quinases de Interação com Receptores/genética
Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo
Proteína de Domínio de Morte Associada a Receptor de TNF/genética
Proteína de Domínio de Morte Associada a Receptor de TNF/metabolismo
Fatores de Virulência/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Escherichia coli Proteins); 0 (FADD protein, human); 0 (Fas-Associated Death Domain Protein); 0 (NleB protein, E coli); 0 (TNF Receptor-Associated Death Domain Protein); 0 (Virulence Factors); EC 2.4.- (Glycosyltransferases); EC 2.7.11.1 (RIPK1 protein, human); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases)
[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:170902
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.805036


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[PMID]:28760932
[Au] Autor:Acuff NV; Li X; Latha K; Nagy T; Watford WT
[Ad] Endereço:Department of Infectious Diseases, University of Georgia, Athens, Georgia, USA.
[Ti] Título:Tpl2 Promotes Innate Cell Recruitment and Effector T Cell Differentiation To Limit Citrobacter rodentium Burden and Dissemination.
[So] Source:Infect Immun;85(10), 2017 Oct.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumor progression locus 2 (Tpl2) is a serine-threonine kinase that regulates Th1 differentiation, secretion of the inflammatory cytokine gamma interferon (IFN-γ), and host defense against the intracellular pathogens , , and However, relatively little is known about the contribution of Tpl2 to Th17 differentiation and immune cell function during infection with an extracellular pathogen. The goal of this study was to determine whether Tpl2 influences the immune response generated to the extracellular bacterium , which induces a mixed Th1 and Th17 response. During peak infection with , mice experienced greater bacterial burdens with evidence of dissemination to the liver and spleen but ultimately cleared the bacteria within 3 weeks postinfection, similar to the findings for wild-type mice. mice also recruited fewer neutrophils and monocytes to the colon during peak infection, which correlated with increased bacterial burdens. In mixed bone marrow chimeras, Tpl2 was shown to play a T cell-intrinsic role in promoting both IFN-γ and interleukin-17A production during infection with However, upon CD4 T cell transfer into mice, CD4 T cells were as protective as wild-type CD4 T cells against the dissemination of bacteria and mortality. These data indicate that the enhanced bacterial burdens in mice are not caused primarily by impairments in CD4 T cell function but result from defects in innate immune cell recruitment and function.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/fisiologia
Citrobacter rodentium/imunologia
Citrobacter rodentium/patogenicidade
Infecções por Enterobacteriaceae/imunologia
Infecções por Enterobacteriaceae/microbiologia
MAP Quinase Quinase Quinases/metabolismo
Proteínas Proto-Oncogênicas/metabolismo
[Mh] Termos MeSH secundário: Animais
Carga Bacteriana
Linfócitos T CD4-Positivos/imunologia
Diferenciação Celular
Gastroenteropatias/imunologia
Gastroenteropatias/microbiologia
Interferon gama/imunologia
Interleucina-17/imunologia
Intestinos/imunologia
Intestinos/microbiologia
MAP Quinase Quinase Quinases/deficiência
MAP Quinase Quinase Quinases/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Neutrófilos/imunologia
Proteínas Proto-Oncogênicas/deficiência
Proteínas Proto-Oncogênicas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-17); 0 (Proto-Oncogene Proteins); 82115-62-6 (Interferon-gamma); EC 2.7.11.25 (MAP Kinase Kinase Kinases); EC 2.7.11.25 (Map3k8 protein, mouse)
[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:170802
[St] Status:MEDLINE


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[PMID]:28694292
[Au] Autor:Diaz LA; Altman NH; Khan W; Serhan CN; Adkins B
[Ad] Endereço:Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, Florida, USA.
[Ti] Título:Specialized Proresolving Mediators Rescue Infant Mice from Lethal Citrobacter rodentium Infection and Promote Immunity against Reinfection.
[So] Source:Infect Immun;85(10), 2017 Oct.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Infants are generally highly susceptible to oral pathogens. Intestinal infection and the associated diarrhea are significant global causes of morbidity and mortality in infants. Among the enteric pathogens, enteropathogenic (EPEC) stands out as showing the highest risk for infection-induced death in infants ≤12 months old. We have developed an experimental model of infant infection with EPEC, using the mouse-specific pathogen Our murine infant model is similar to EPEC infection in human infants since infant mice are much more susceptible to infection than adult mice; infants infected with 50-fold fewer bacteria than the standard adult dose uniformly succumbed to the infection. Infant infection is characterized by high early and sustained bacterial titers and profound intestinal inflammation associated with extensive necrosis and systemic dissemination of the bacteria. Therefore, it seems likely that infant deaths result from sepsis secondary to intestinal damage. Recently, specialized proresolving mediators (SPM) have been found to exert profound beneficial effects in adult models of infection. Thus, we investigated the actions of two proresolving lipid mediators, resolvin D1 (RvD1) and resolvin D5 (RvD5), on the course of infection in infants. Strikingly, postinfection treatment with RvD1 and RvD5 reduced bacterial loads, mitigated inflammation, and rescued the infants from death. Furthermore, postinfection treatment with RvD1 and RvD5 led to protection from reinfection associated with -specific IgG responses comparable to those in adults. These results indicate that SPM may provide novel therapeutic tools for the treatment of pathological intestinal infections in infants.
[Mh] Termos MeSH primário: Citrobacter rodentium/imunologia
Citrobacter rodentium/patogenicidade
Ácidos Docosa-Hexaenoicos/uso terapêutico
Infecções por Enterobacteriaceae/imunologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Carga Bacteriana
Colite/complicações
Colite/tratamento farmacológico
Colite/microbiologia
Diarreia/microbiologia
Modelos Animais de Doenças
Ácidos Docosa-Hexaenoicos/administração & dosagem
Infecções por Enterobacteriaceae/tratamento farmacológico
Infecções por Enterobacteriaceae/microbiologia
Intestinos/efeitos dos fármacos
Intestinos/imunologia
Intestinos/microbiologia
Camundongos
Camundongos Endogâmicos C57BL
Recidiva
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (resolvin D1); 0 (resolvin D5); 25167-62-8 (Docosahexaenoic Acids)
[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]:28662171
[Au] Autor:Buschor S; Cuenca M; Uster SS; Schären OP; Balmer ML; Terrazos MA; Schürch CM; Hapfelmeier S
[Ad] Endereço:Institute for Infectious Diseases, University of Bern, Bern, Switzerland.
[Ti] Título:Innate immunity restricts Citrobacter rodentium A/E pathogenesis initiation to an early window of opportunity.
[So] Source:PLoS Pathog;13(6):e1006476, 2017 Jun.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Citrobacter rodentium infection is a mouse model for the important human diarrheal infection caused by enteropathogenic E. coli (EPEC). The pathogenesis of both species is very similar and depends on their unique ability to form intimately epithelium-adherent microcolonies, also known as "attachment/effacement" (A/E) lesions. These microcolonies must be dynamic and able to self-renew by continuous re-infection of the rapidly regenerating epithelium. It is unknown whether sustained epithelial A/E lesion pathogenesis is achieved through re-infection by planktonic bacteria from the luminal compartment or local spread of sessile bacteria without a planktonic phase. Focusing on the earliest events as C. rodentium becomes established, we show here that all colonic epithelial A/E microcolonies are clonal bacterial populations, and thus depend on local clonal growth to persist. In wild-type mice, microcolonies are established exclusively within the first 18 hours of infection. These early events shape the ongoing intestinal geography and severity of infection despite the continuous presence of phenotypically virulent luminal bacteria. Mechanistically, induced resistance to A/E lesion de-novo formation is mediated by TLR-MyD88/Trif-dependent signaling and is induced specifically by virulent C. rodentium in a virulence gene-dependent manner. Our data demonstrate that the establishment phase of C. rodentium pathogenesis in vivo is restricted to a very short window of opportunity that determines both disease geography and severity.
[Mh] Termos MeSH primário: Citrobacter rodentium/imunologia
Infecções por Enterobacteriaceae/imunologia
Imunidade Inata/imunologia
[Mh] Termos MeSH secundário: Animais
Citrobacter rodentium/patogenicidade
Colo/microbiologia
Modelos Animais de Doenças
Escherichia coli Enteropatogênica/imunologia
Escherichia coli Enteropatogênica/patogenicidade
Proteínas de Escherichia coli/metabolismo
Camundongos Endogâmicos C57BL
Virulência/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Escherichia coli Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170630
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006476


  5 / 425 MEDLINE  
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[PMID]:28522607
[Au] Autor:El Qaidi S; Chen K; Halim A; Siukstaite L; Rueter C; Hurtado-Guerrero R; Clausen H; Hardwidge PR
[Ad] Endereço:From the College of Veterinary Medicine, Kansas State University, Manhattan, Kansas 66506.
[Ti] Título:NleB/SseK effectors from , , and display distinct differences in host substrate specificity.
[So] Source:J Biol Chem;292(27):11423-11430, 2017 Jul 07.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Many Gram-negative bacterial pathogens use a syringe-like apparatus called a type III secretion system to inject virulence factors into host cells. Some of these effectors are enzymes that modify host proteins to subvert their normal functions. NleB is a glycosyltransferase that modifies host proteins with -acetyl-d-glucosamine to inhibit antibacterial and inflammatory host responses. NleB is conserved among the attaching/effacing pathogens enterohemorrhagic (EHEC), enteropathogenic (EPEC), and Moreover, strains encode up to three NleB orthologs named SseK1, SseK2, and SseK3. However, there are conflicting reports regarding the activities and host protein targets among the NleB/SseK orthologs. Therefore, here we performed glycosylation assays and cell culture experiments to compare the activities and substrate specificities of these effectors. SseK1, SseK3, EHEC NleB1, EPEC NleB1, and NleB blocked TNF-mediated NF-κB pathway activation, whereas SseK2 and NleB2 did not. NleB, EHEC NleB1, and SseK1 glycosylated host GAPDH. NleB, EHEC NleB1, EPEC NleB1, and SseK2 glycosylated the FADD (Fas-associated death domain protein). SseK3 and NleB2 were not active against either substrate. We also found that EHEC NleB1 glycosylated two GAPDH arginine residues, Arg and Arg , and that these two residues were essential for GAPDH-mediated activation of TNF receptor-associated factor 2 ubiquitination. These results provide evidence that members of this highly conserved family of bacterial virulence effectors target different host protein substrates and exhibit distinct cellular modes of action to suppress host responses.
[Mh] Termos MeSH primário: Proteínas de Bactérias/metabolismo
Citrobacter rodentium/enzimologia
Escherichia coli Êntero-Hemorrágica/enzimologia
Escherichia coli Enteropatogênica/enzimologia
Proteínas de Escherichia coli/metabolismo
Salmonella enterica/enzimologia
Fatores de Virulência/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas de Bactérias/genética
Citrobacter rodentium/genética
Citrobacter rodentium/patogenicidade
Escherichia coli Êntero-Hemorrágica/genética
Escherichia coli Êntero-Hemorrágica/patogenicidade
Escherichia coli Enteropatogênica/genética
Escherichia coli Enteropatogênica/patogenicidade
Proteínas de Escherichia coli/genética
Proteína de Domínio de Morte Associada a Fas/genética
Proteína de Domínio de Morte Associada a Fas/metabolismo
Gliceraldeído-3-Fosfato Desidrogenases/genética
Gliceraldeído-3-Fosfato Desidrogenases/metabolismo
Glicosilação
Camundongos
Células RAW 264.7
Receptores Tipo II do Fator de Necrose Tumoral/genética
Receptores Tipo II do Fator de Necrose Tumoral/metabolismo
Salmonella enterica/genética
Salmonella enterica/patogenicidade
Fator 2 Associado a Receptor de TNF/genética
Fator 2 Associado a Receptor de TNF/metabolismo
Ubiquitinação
Fatores de Virulência/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Escherichia coli Proteins); 0 (Fadd protein, mouse); 0 (Fas-Associated Death Domain Protein); 0 (NleB protein, E coli); 0 (Receptors, Tumor Necrosis Factor, Type II); 0 (SseK1 protein, Salmonella enterica); 0 (SseK2 protein, Salmonella enterica); 0 (TNF Receptor-Associated Factor 2); 0 (Virulence Factors); EC 1.2.1.- (Glyceraldehyde-3-Phosphate Dehydrogenases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170520
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.790675


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[PMID]:28520792
[Au] Autor:Friedrich C; Mamareli P; Thiemann S; Kruse F; Wang Z; Holzmann B; Strowig T; Sparwasser T; Lochner M
[Ad] Endereço:Institute of Infection Immunology, TWINCORE, Centre for Experimental and Clinical Infection Research; a joint venture between the Medical School Hannover (MHH) and the Helmholtz Centre for Infection Research (HZI), Hannover, Germany.
[Ti] Título:MyD88 signaling in dendritic cells and the intestinal epithelium controls immunity against intestinal infection with C. rodentium.
[So] Source:PLoS Pathog;13(5):e1006357, 2017 May.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:MyD88-mediated signaling downstream of Toll-like receptors and the IL-1 receptor family is critically involved in the induction of protective host responses upon infections. Although it is known that MyD88-deficient mice are highly susceptible to a wide range of bacterial infections, the cell type-specific contribution of MyD88 in protecting the host against intestinal bacterial infection is only poorly understood. In order to investigate the importance of MyD88 in specific immune and nonimmune cell types during intestinal infection, we employed a novel murine knock-in model for MyD88 that enables the cell type-specific reactivation of functional MyD88 expression in otherwise MyD88-deficient mice. We report here that functional MyD88 signaling in CD11c+ cells was sufficient to activate intestinal dendritic cells (DC) and to induce the early group 3 innate lymphoid cell (ILC3) response as well as the development of colonic Th17/Th1 cells in response to infection with the intestinal pathogen C. rodentium. In contrast, restricting MyD88 signaling to several other cell types, including macrophages (MO), T cells or ILC3 did not induce efficient intestinal immune responses upon infection. However, we observed that the functional expression of MyD88 in intestinal epithelial cells (IEC) also partially protected the mice during intestinal infection, which was associated with enhanced epithelial barrier integrity and increased expression of the antimicrobial peptide RegIIIγ and the acute phase protein SAA1 by epithelial cells. Together, our data suggest that MyD88 signaling in DC and IEC is both essential and sufficient to induce a full spectrum of host responses upon intestinal infection with C. rodentium.
[Mh] Termos MeSH primário: Citrobacter rodentium/imunologia
Infecções por Enterobacteriaceae/imunologia
Fator 88 de Diferenciação Mieloide/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Colo/imunologia
Colo/microbiologia
Células Dendríticas/imunologia
Células Dendríticas/microbiologia
Infecções por Enterobacteriaceae/microbiologia
Infecções por Enterobacteriaceae/patologia
Células Epiteliais/imunologia
Células Epiteliais/microbiologia
Técnicas de Introdução de Genes
Mucosa Intestinal/imunologia
Mucosa Intestinal/microbiologia
Macrófagos/imunologia
Macrófagos/microbiologia
Camundongos
Camundongos Endogâmicos C57BL
Fator 88 de Diferenciação Mieloide/genética
Receptores de Interleucina-1/metabolismo
Células Th1/imunologia
Células Th1/microbiologia
Células Th17/imunologia
Células Th17/microbiologia
Receptores Toll-Like/genética
Receptores Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Myd88 protein, mouse); 0 (Myeloid Differentiation Factor 88); 0 (Receptors, Interleukin-1); 0 (Toll-Like Receptors)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006357


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[PMID]:28356548
[Au] Autor:Nunez G
[Ad] Endereço:Department of Pathology and Comprehensive Cancer Center, University of Michigan, Michigan, USA.
[Ti] Título:Linking Pathogen Virulence, Host Immunity and The Microbiota at the Intestinal Barrier.
[So] Source:Keio J Med;66(1):14, 2017.
[Is] ISSN:1880-1293
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The mechanisms that allow enteric pathogens to colonize the intestine and host immunity as well as the indigenous microbiota to inhibit pathogen colonization remain poorly understood. Our laboratory is using Citrobacter rodentium, a mouse pathogen that models human infections by enteropathogenic E. coli, to understand the mechanisms that regulate the colonization and clearance of the pathogen in the gut. These studies have revealed how the pathogen colonizes and replicates successfully early during infection and how host immunity and the indigenous microbiota cooperate to eradicate the pathogen in the later stage of the infection. The impairment of the immune system to control the barrier function of the intestine leads to pathogen invasion and the induction of a second layer of host protective immunity to limit the systemic spread of the pathogen.(Presented at the 1931st Meeting, January 17, 2017).
[Mh] Termos MeSH primário: Citrobacter rodentium/patogenicidade
Infecções por Enterobacteriaceae/imunologia
Escherichia coli Enteropatogênica/patogenicidade
Microbioma Gastrointestinal/imunologia
Imunidade Inata
Mucosa Intestinal/imunologia
[Mh] Termos MeSH secundário: Animais
Citrobacter rodentium/crescimento & desenvolvimento
Citrobacter rodentium/imunologia
Modelos Animais de Doenças
Infecções por Enterobacteriaceae/microbiologia
Escherichia coli Enteropatogênica/crescimento & desenvolvimento
Escherichia coli Enteropatogênica/imunologia
Interações Hospedeiro-Patógeno
Seres Humanos
Mucosa Intestinal/microbiologia
Camundongos
Virulência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE
[do] DOI:10.2302/kjm.66-001-ABST


  8 / 425 MEDLINE  
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[PMID]:28356348
[Au] Autor:Acuff NV; Li X; Elmore J; Rada B; Watford WT
[Ad] Endereço:Department of Infectious Diseases, University of Georgia, Athens, Georgia, USA.
[Ti] Título:Tpl2 promotes neutrophil trafficking, oxidative burst, and bacterial killing.
[So] Source:J Leukoc Biol;101(6):1325-1333, 2017 Jun.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumor progression locus 2 (Tpl2) is a serine/threonine kinase that promotes inflammatory cytokine production by activating the MEK/ERK pathway. Tpl2 has been shown to be important for eliciting the inflammatory properties of macrophages; however, there is relatively little known about the contribution of Tpl2 to neutrophil effector functions. This is an important consideration, as neutrophils provide the first line of defense against infection in the innate immune system. We found that Tpl2 is expressed in both human and murine neutrophils, suggesting a potential function for Tpl2 in this lineage. Despite significantly higher proportions of bone marrow (BM) neutrophils in Tpl2-deficient ( ) mice compared with wild-type (WT) mice, mice have significantly reduced proportions of circulating neutrophils. neutrophils show impaired recruitment to thioglycollate, which was primarily a result of neutrophil-extrinsic factors in the host. In response to infection, neutrophils secrete inflammatory cytokines and produce reactive oxygen species (ROS), which promote bacterial killing. Tpl2 ablation impaired neutrophil TNF secretion in response to LPS stimulation, superoxide generation in response to the chemotactic peptide fMLP, and killing of the extracellular bacterium, , despite normal bacterial phagocytosis. These results implicate Tpl2 in the regulation of multiple neutrophil antimicrobial pathways, including inflammatory cytokine secretion and oxidative burst. Furthermore, they indicate that Tpl2 functions early during infection to bolster neutrophil-mediated innate immunity against extracellular bacteria.
[Mh] Termos MeSH primário: Citrobacter rodentium/imunologia
Infecções por Enterobacteriaceae/imunologia
Imunidade Inata/imunologia
MAP Quinase Quinase Quinases/fisiologia
Macrófagos/imunologia
Neutrófilos/imunologia
Proteínas Proto-Oncogênicas/fisiologia
Explosão Respiratória/imunologia
[Mh] Termos MeSH secundário: Animais
Movimento Celular
Infecções por Enterobacteriaceae/metabolismo
Infecções por Enterobacteriaceae/microbiologia
Feminino
Seres Humanos
Macrófagos/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Neutrófilos/metabolismo
Fagocitose
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins); 0 (Reactive Oxygen Species); EC 2.7.11.25 (MAP Kinase Kinase Kinases); EC 2.7.11.25 (Map3k8 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.3A0316-146R


  9 / 425 MEDLINE  
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[PMID]:28348052
[Au] Autor:Tremblay S; Romain G; Roux M; Chen XL; Brown K; Gibson DL; Ramanathan S; Menendez A
[Ad] Endereço:Department of Microbiology and Infectious Diseases, Université de Sherbrooke, Sherbrooke, Québec, Canada.
[Ti] Título:Bile Acid Administration Elicits an Intestinal Antimicrobial Program and Reduces the Bacterial Burden in Two Mouse Models of Enteric Infection.
[So] Source:Infect Immun;85(6), 2017 Jun.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In addition to their chemical antimicrobial nature, bile acids are thought to have other functions in the homeostatic control of gastrointestinal immunity. However, those functions have remained largely undefined. In this work, we used ileal explants and mouse models of bile acid administration to investigate the role of bile acids in the regulation of the intestinal antimicrobial response. Mice fed on a diet supplemented with 0.1% chenodeoxycholic acid (CDCA) showed an upregulated expression of Paneth cell α-defensins as well as an increased synthesis of the type-C lectins Reg3b and Reg3g by the ileal epithelium. CDCA acted on several epithelial cell types, by a mechanism independent from farnesoid X receptor (FXR) and not involving STAT3 or ß-catenin activation. CDCA feeding did not change the relative abundance of major commensal bacterial groups of the ileum, as shown by 16S analyses. However, administration of CDCA increased the expression of ileal and induced a change in the composition of the mucosal immune cell repertoire, decreasing the proportion of Ly6G and CD68 cells, while increasing the relative amount of IgGκ B cells. Oral administration of CDCA to mice attenuated infections with the bile-resistant pathogens serovar Typhimurium and , promoting lower systemic colonization and faster bacteria clearance, respectively. Our results demonstrate that bile acid signaling in the ileum triggers an antimicrobial program that can be potentially used as a therapeutic option against intestinal bacterial infections.
[Mh] Termos MeSH primário: Ácido Quenodesoxicólico/administração & dosagem
Infecções por Enterobacteriaceae/imunologia
Íleo/microbiologia
Imunidade nas Mucosas
Infecções por Salmonella/imunologia
alfa-Defensinas/imunologia
[Mh] Termos MeSH secundário: Animais
Carga Bacteriana
Citrobacter rodentium/efeitos dos fármacos
Íleo/imunologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Celulas de Paneth/imunologia
Celulas de Paneth/microbiologia
Salmonella typhimurium/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (alpha-Defensins); 0GEI24LG0J (Chenodeoxycholic Acid)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171123
[Lr] Data última revisão:
171123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE


  10 / 425 MEDLINE  
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[PMID]:28333177
[Au] Autor:Waki N; Kuwabara Y; Yoshikawa Y; Suganuma H; Koide H; Oku N; Ohashi N
[Ad] Endereço:Innovation Division, KAGOME CO., LTD., 17 Nishitomiyama, Nasushiobara, Tochigi 329-2762, Japan.
[Ti] Título:Amelioration of Citrobacter rodentium proliferation in early stage of infection in mice by pretreatment with Lactobacillus brevis KB290 and verification using in vivo bioluminescence imaging.
[So] Source:FEMS Microbiol Lett;364(6), 2017 Mar 01.
[Is] ISSN:1574-6968
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Bioluminescent imaging (BLI) has become a useful tool for monitoring bacterial infections in real time. Citrobacter rodentium and its BLI are widely used as a murine model of enteropathogenic and enterohaemorrhagic Escherichia coli infection. In this study, we evaluated the protective effects of the probiotic Lactobacillus brevis KB290 against C. rodentium infection by the BLI approach. First, we examined several solutions for making the suspension of bioluminescent C. rodentium for an oral inoculation to establish a stable intestinal infection. Three percent NaHCO3 solution was found to be the best. Subsequently, mice were orally administered KB290 once daily for 7 days before inoculation with bioluminescent C. rodentium and for 8 days after infection. The bioluminescence intensity of mice fed with KB290 was significantly lower than that of unfed mice on days 1-3 after infection. The mRNA levels of tumour necrosis factor-α and interferon-γ in the distal colon from KB290-fed mice were shown to be significantly higher than those from unfed mice on day 3 after infection. The results suggested that KB290 intake partially inhibited the proliferation of C. rodentium, especially in the early stages of infection, viathe moderate enhancement of tumour necrosis factor-α and interferon-γ production in the colon.
[Mh] Termos MeSH primário: Antibiose
Citrobacter rodentium/fisiologia
Infecções por Enterobacteriaceae/diagnóstico por imagem
Infecções por Enterobacteriaceae/microbiologia
Lactobacillus brevis/fisiologia
Medições Luminescentes
[Mh] Termos MeSH secundário: Animais
Colo/metabolismo
Colo/microbiologia
Colo/patologia
Citocinas/genética
Citocinas/metabolismo
Infecções por Enterobacteriaceae/genética
Infecções por Enterobacteriaceae/metabolismo
Feminino
Expressão Gênica
Mediadores da Inflamação/metabolismo
Medições Luminescentes/métodos
Camundongos
Probióticos/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Inflammation Mediators)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE
[do] DOI:10.1093/femsle/fnw254



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