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[PMID]:28458362
[Au] Autor:Tanaka K; Yoshitomi T; Hirahara K
[Ad] Endereço:Biologics & Immuno-Oncology Laboratories, Daiichi Sankyo Co., Ltd.
[Ti] Título:Elucidation of Distinct Roles of Guinea Pig CXCR1 and CXCR2 in Neutrophil Migration toward IL-8 and GROα by Specific Antibodies.
[So] Source:Biol Pharm Bull;40(5):729-732, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Chemokine receptors CXCR1 and CXCR2 are conserved between guinea pigs and humans, but the distinct role of each receptor in chemotactic responses of neutrophils against chemokine ligands has not been elucidated due in part to the lack of specific inhibitors against these receptors in guinea pigs. In this study, we investigated the roles of guinea pig CXCR1 and CXCR2 on neutrophils in chemotactic responses to guinea pig interleukin (IL)-8 and growth-regulated oncogene (GRO)α by using specific inhibitory antibodies against these receptors. Neutrophil migration induced by IL-8 was partially inhibited by either anti-CXCR1 antibody or anti-CXCR2 antibody. In addition, the migration was inhibited completely when both anti-CXCR1 and anti-CXCR2 antibodies were combined. On the other hand, neutrophil migration induced by GROα was not inhibited by anti-CXCR1 antibody while inhibited profoundly by anti-CXCR2 antibody. These results indicated that CXCR1 and CXCR2 mediated migration induced by the IL-8 synergistically and only CXCR2 mediated migration induced by GROα in guinea pig neutrophils. Our findings on ligand selectivity of CXCR1 and CXCR2 in guinea pigs are consistent with those in humans.
[Mh] Termos MeSH primário: Quimiocina CXCL1/farmacologia
Interleucina-8/farmacologia
Neutrófilos/fisiologia
Receptores de Interleucina-8A/fisiologia
Receptores de Interleucina-8B/fisiologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Bloqueadores/farmacologia
Movimento Celular/efeitos dos fármacos
Quimiocina CXCL1/antagonistas & inibidores
Quimiotaxia/efeitos dos fármacos
Feminino
Cobaias
Doenças do Sistema Imune
Interleucina-8/antagonistas & inibidores
Transtornos Leucocíticos
Neutrófilos/imunologia
Receptores de Interleucina-8A/imunologia
Receptores de Interleucina-8B/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Blocking); 0 (Chemokine CXCL1); 0 (Interleukin-8); 0 (Receptors, Interleukin-8A); 0 (Receptors, Interleukin-8B)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-00918


  2 / 1257 MEDLINE  
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[PMID]:28450382
[Au] Autor:Young HL; Rowling EJ; Bugatti M; Giurisato E; Luheshi N; Arozarena I; Acosta JC; Kamarashev J; Frederick DT; Cooper ZA; Reuben A; Gil J; Flaherty KT; Wargo JA; Vermi W; Smith MP; Wellbrock C; Hurlstone A
[Ad] Endereço:Manchester Cancer Research Centre, Faculty of Biology, Medicine, and Health, School of Medical Sciences, Division of Molecular and Clinical Cancer Studies, The University of Manchester, Manchester M13 9PT, England, UK.
[Ti] Título:An adaptive signaling network in melanoma inflammatory niches confers tolerance to MAPK signaling inhibition.
[So] Source:J Exp Med;214(6):1691-1710, 2017 Jun 05.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitogen-activated protein kinase (MAPK) pathway antagonists induce profound clinical responses in advanced cutaneous melanoma, but complete remissions are frustrated by the development of acquired resistance. Before resistance emerges, adaptive responses establish a mutation-independent drug tolerance. Antagonizing these adaptive responses could improve drug effects, thereby thwarting the emergence of acquired resistance. In this study, we reveal that inflammatory niches consisting of tumor-associated macrophages and fibroblasts contribute to treatment tolerance through a cytokine-signaling network that involves macrophage-derived IL-1ß and fibroblast-derived CXCR2 ligands. Fibroblasts require IL-1ß to produce CXCR2 ligands, and loss of host IL-1R signaling in vivo reduces melanoma growth. In tumors from patients on treatment, signaling from inflammatory niches is amplified in the presence of MAPK inhibitors. Signaling from inflammatory niches counteracts combined BRAF/MEK (MAPK/extracellular signal-regulated kinase kinase) inhibitor treatment, and consequently, inhibiting IL-1R or CXCR2 signaling in vivo enhanced the efficacy of MAPK inhibitors. We conclude that melanoma inflammatory niches adapt to and confer drug tolerance toward BRAF and MEK inhibitors early during treatment.
[Mh] Termos MeSH primário: Inflamação/enzimologia
Inflamação/patologia
Sistema de Sinalização das MAP Quinases
Melanoma/enzimologia
Melanoma/patologia
Neoplasias Cutâneas/enzimologia
Neoplasias Cutâneas/patologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Quimiocina CXCL1/metabolismo
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Seres Humanos
Interleucina-1/metabolismo
Interleucina-1beta/metabolismo
Interleucina-8/metabolismo
Ligantes
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Camundongos Knockout
Quinases de Proteína Quinase Ativadas por Mitógeno/antagonistas & inibidores
Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo
NF-kappa B/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas B-raf/metabolismo
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Receptores de Interleucina-1/metabolismo
Receptores de Interleucina-8B/metabolismo
Células Estromais/metabolismo
Células Estromais/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL1); 0 (Interleukin-1); 0 (Interleukin-1beta); 0 (Interleukin-8); 0 (Ligands); 0 (NF-kappa B); 0 (Protein Kinase Inhibitors); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Receptors, Interleukin-1); 0 (Receptors, Interleukin-8B); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf); EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180125
[Lr] Data última revisão:
180125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20160855


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[PMID]:28743719
[Au] Autor:Del Prete A; Martínez-Muñoz L; Mazzon C; Toffali L; Sozio F; Za L; Bosisio D; Gazzurelli L; Salvi V; Tiberio L; Liberati C; Scanziani E; Vecchi A; Laudanna C; Mellado M; Mantovani A; Sozzani S
[Ad] Endereço:Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
[Ti] Título:The atypical receptor CCRL2 is required for CXCR2-dependent neutrophil recruitment and tissue damage.
[So] Source:Blood;130(10):1223-1234, 2017 09 07.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CCRL2 is a 7-transmembrane domain receptor that shares structural and functional similarities with the family of atypical chemokine receptors (ACKRs). CCRL2 is upregulated by inflammatory signals and, unlike other ACKRs, it is not a chemoattractant-scavenging receptor, does not activate ß-arrestins, and is widely expressed by many leukocyte subsets. Therefore, the biological role of CCRL2 in immunity is still unclear. We report that CCRL2-deficient mice have a defect in neutrophil recruitment and are protected in 2 models of inflammatory arthritis. In vitro, CCRL2 was found to constitutively form homodimers and heterodimers with CXCR2, a main neutrophil chemotactic receptor. By heterodimerization, CCRL2 could regulate membrane expression and promote CXCR2 functions, including the activation of ß2-integrins. Therefore, upregulation of CCRL2 observed under inflammatory conditions is functional to finely tune CXCR2-mediated neutrophil recruitment at sites of inflammation.
[Mh] Termos MeSH primário: Artrite/metabolismo
Artrite/patologia
Neutrófilos/patologia
Receptores de Quimiocinas/metabolismo
Receptores de Interleucina-8B/metabolismo
[Mh] Termos MeSH secundário: Animais
Artrite/complicações
Antígenos CD18/metabolismo
Sobrevivência Celular
Modelos Animais de Doenças
Inflamação/complicações
Inflamação/patologia
Camundongos Knockout
Infiltração de Neutrófilos
Conformação Proteica
Multimerização Proteica
Receptores de Quimiocinas/química
Receptores de Quimiocinas/deficiência
Receptores de Interleucina-8B/química
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD18 Antigens); 0 (Ccrl2 protein, mouse); 0 (Receptors, Chemokine); 0 (Receptors, Interleukin-8B)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180113
[Lr] Data última revisão:
180113
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-04-777680


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[PMID]:28964785
[Au] Autor:Xu H; Lin F; Wang Z; Yang L; Meng J; Ou Z; Shao Z; Di G; Yang G
[Ad] Endereço:Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Department of Oncology, Shanghai Medical College, Fudan University, 200032, China.
[Ti] Título:CXCR2 promotes breast cancer metastasis and chemoresistance via suppression of AKT1 and activation of COX2.
[So] Source:Cancer Lett;412:69-80, 2018 Jan 01.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Metastasis and chemoresistance are two major causes of breast cancer death. We show here that the chemokine receptor CXCR2 was overexpressed in breast cancer cell lines and tissues. CXCR2 promoted anti-apoptosis, anti-senescence, and epithelial-to-mesenchymal transition (EMT) of breast cancer cells, leading to the enhanced metastasis and chemoresistance. Further study suggested that AKT1 and cyclooxygenase-2 (COX2; PTGS2) might mediate the CXCR2 signaling to inversely control the breast cancer metastasis and chemoresistance through the regulation of EMT, apoptosis, and senescence. Analyses of clinical data indicate that the high expression of CXCR2 was correlated with the high expression of COX2 and the low expression of AKT1, P85α, E-cadherin, and ß-catenin in cancer tissues. Poor outcomes were associated with the high expression of CXCR2 or COX2 while favorable survivals were associated with the high expression of P85α, AKT1, or E-cadherin in all cancer patients. Cox multivariate analysis demonstrated that CXCR2, COX2, and AKT1 could be independent predictors for disease free survivals. All these data suggest that CXCR2 promotes breast cancer metastasis and chemoresistance via suppressing AKT1 and activating COX2. Thus, antagonists of the CXCR2 signaling molecules may be used to treat breast cancer patients particularly with high metastasis and chemoresistance.
[Mh] Termos MeSH primário: Neoplasias da Mama/patologia
Ciclo-Oxigenase 2/fisiologia
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Receptores de Interleucina-8B/fisiologia
[Mh] Termos MeSH secundário: Apoptose
Neoplasias da Mama/tratamento farmacológico
Neoplasias da Mama/mortalidade
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Resistência a Medicamentos Antineoplásicos
Transição Epitelial-Mesenquimal
Feminino
Seres Humanos
Proteínas Proto-Oncogênicas c-akt/fisiologia
Receptores de Interleucina-8B/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Interleukin-8B); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (PTGS2 protein, human); EC 2.7.11.1 (AKT1 protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171205
[Lr] Data última revisão:
171205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171002
[St] Status:MEDLINE


  5 / 1257 MEDLINE  
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[PMID]:28865993
[Au] Autor:Frieler RA; Chung Y; Ahlers CG; Gheordunescu G; Song J; Vigil TM; Shah YM; Mortensen RM
[Ad] Endereço:Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48109, United States. Electronic address: rfrieler@umich.edu.
[Ti] Título:Genetic neutrophil deficiency ameliorates cerebral ischemia-reperfusion injury.
[So] Source:Exp Neurol;298(Pt A):104-111, 2017 Dec.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neutrophils respond rapidly to cerebral ischemia and are thought to contribute to inflammation-mediated injury during stroke. Using myeloid Mcl1 knockout mice as a model of genetic neutrophil deficiency, we investigated the contribution of neutrophils to stroke pathophysiology. Myeloid Mcl1 knockout mice were subjected to transient middle cerebral artery occlusion and infarct size was assessed by MRI after 24h reperfusion. Immune cell mobilization and infiltration was assessed by flow cytometry. We found that myeloid Mcl1 knockout mice had significantly reduced infarct size when compared to heterozygous and wild type control mice (MyMcl1 : 78.0mm ; MyMcl1 : 83.4mm ; MyMcl1 : 55.1mm ). This was accompanied by a nearly complete absence of neutrophils in the ischemic hemisphere of myeloid Mcl1 knockout mice. Although myeloid Mcl1 knockout mice were protected from cerebral infarction, no significant differences in neurological deficit or the mRNA expression of inflammatory genes (TNFα, IL-1ß, and MCP1) were detected. Inhibition of neutrophil chemotaxis using CXCR2 pepducin treatment partially reduced neutrophil mobilization and recruitment to the brain after stroke, but did not reduce infarct size 24h after transient MCA occlusion. These data confirm that neutrophils have an important role in infarct development during stroke pathophysiology, and suggest that complete deficiency, but not partial inhibition, is necessary to prevent neutrophil-mediated injury during stroke.
[Mh] Termos MeSH primário: Isquemia Encefálica/genética
Isquemia Encefálica/metabolismo
Proteína de Sequência 1 de Leucemia de Células Mieloides/genética
Neutrófilos/fisiologia
Traumatismo por Reperfusão/genética
Traumatismo por Reperfusão/metabolismo
[Mh] Termos MeSH secundário: Animais
Isquemia Encefálica/prevenção & controle
Quimiotaxia/fisiologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteína de Sequência 1 de Leucemia de Células Mieloides/deficiência
Receptores de Interleucina-8B/genética
Receptores de Interleucina-8B/metabolismo
Traumatismo por Reperfusão/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mcl1 protein, mouse); 0 (Myeloid Cell Leukemia Sequence 1 Protein); 0 (Receptors, Interleukin-8B)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170904
[St] Status:MEDLINE


  6 / 1257 MEDLINE  
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[PMID]:28823917
[Au] Autor:Shih CH; Chiang TB; Wang WJ
[Ad] Endereço:Chang Gung University of Science and Technology, Guishan Dist., Taoyuan City, Taiwan.
[Ti] Título:Synergistic suppression of a disintegrin acurhagin-C in combination with AZD4547 and reparixin on terminating development for human osteosarcoma MG-63 cell.
[So] Source:Biochem Biophys Res Commun;492(3):513-519, 2017 Oct 21.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Current therapies available for the treatment of human osteosarcoma, an aggressive bone tumor, are insufficient. To examine an alternative approach of integrin-based anti-osteosacoma strategy, acurhagin-C, a Glu-Cys-Asp (ECD)-disintegrin, was isolated and evaluated for its application in combination with two potent inhibitors of basic fibroblast growth factor (bFGF) and interleukin-8 (IL-8). The investigation of human osteosarcoma MG-63 cells pre-incubated with a FGF receptor-1 (FGFR-1) blocker AZD4547, a CXC-chemokine receptor-1/-2 (CXCR1/2) antagonist reparixin, and acurhagin-C via two given modes of separation and combination was executed. Detected by flow cytometry, integrins-α2/-α5/-αv/-ß1, FGFR-1, CXCR1 and CXCR2 constitutively express on the resting membrane. However, bFGF/IL-8-activated MG-63 cells only statistically enhanced the surface exposure of integrins-α5/-ß1, FGFR-1 and CXCR2. In activated MG-63 cells, acurhagin-C targeting integrin-α5 not only might potentiate the inhibitory effect of AZD4547 and reparixin on the surface expression of integrin-α5, FGFR-1 and CXCR2, but also acurhagin-C used alone remained effectively to diminish the surface exposure of those targeted receptors. Hence, a complicated crosstalk mechanism should be involved in the membrane interactions. Furthermore, co-administration of acurhagin-C with AZD4547 and reparixin also showed to have the synergistic suppression toward cell proliferation and the gene expression of matrix metalloproteinase-2. Also, the administration of three-in-one mode could nearly abrogate the cellular attachment onto collagen-IV- and fibronectin-coated wells, as well as penetration into Matrigel-barrier. These data supported an ECD-disintegrin acurhagin-C targeting integrin-α5 upon combined used with AZD4547 and reparixin may become a promising therapeutic approach for attenuating osteosarcoma development.
[Mh] Termos MeSH primário: Benzamidas/farmacologia
Desintegrinas/farmacologia
Osteossarcoma/tratamento farmacológico
Osteossarcoma/patologia
Piperazinas/farmacologia
Pirazóis/farmacologia
Sulfonamidas/farmacologia
[Mh] Termos MeSH secundário: Benzamidas/química
Proliferação Celular/efeitos dos fármacos
Desintegrinas/química
Desintegrinas/isolamento & purificação
Seres Humanos
Piperazinas/química
Pirazóis/química
Receptor Tipo 1 de Fator de Crescimento de Fibroblastos/antagonistas & inibidores
Receptor Tipo 1 de Fator de Crescimento de Fibroblastos/metabolismo
Receptores de Interleucina-8B/antagonistas & inibidores
Receptores de Interleucina-8B/metabolismo
Sulfonamidas/química
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(4-isobutylphenyl)propionylmethanesulfonamide); 0 (AZD4547); 0 (Benzamides); 0 (Disintegrins); 0 (Piperazines); 0 (Pyrazoles); 0 (Receptors, Interleukin-8B); 0 (Sulfonamides); EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 1)
[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:170822
[St] Status:MEDLINE


  7 / 1257 MEDLINE  
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[PMID]:28817707
[Au] Autor:Watanabe K; Gilchrist CA; Uddin MJ; Burgess SL; Abhyankar MM; Moonah SN; Noor Z; Donowitz JR; Schneider BN; Arju T; Ahmed E; Kabir M; Alam M; Haque R; Pramoonjago P; Mehrad B; Petri WA
[Ad] Endereço:Division of Infectious Diseases and International Health, Department of Medicine, University of Virginia, Charlottesville, Virginia, United States of America.
[Ti] Título:Microbiome-mediated neutrophil recruitment via CXCR2 and protection from amebic colitis.
[So] Source:PLoS Pathog;13(8):e1006513, 2017 Aug.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The disease severity of Entamoeba histolytica infection ranges from asymptomatic to life-threatening. Recent human and animal data implicate the gut microbiome as a modifier of E. histolytica virulence. Here we have explored the association of the microbiome with susceptibility to amebiasis in infants and in the mouse model of amebic colitis. Dysbiosis occurred symptomatic E. histolytica infection in children, as evidenced by a lower Shannon diversity index of the gut microbiota. To test if dysbiosis was a cause of susceptibility, wild type C57BL/6 mice (which are innately resistant to E. histiolytica infection) were treated with antibiotics prior to cecal challenge with E. histolytica. Compared with untreated mice, antibiotic pre-treated mice had more severe colitis and delayed clearance of E. histolytica. Gut IL-25 and mucus protein Muc2, both shown to provide innate immunity in the mouse model of amebic colitis, were lower in antibiotic pre-treated mice. Moreover, dysbiotic mice had fewer cecal neutrophils and myeloperoxidase activity. Paradoxically, the neutrophil chemoattractant chemokines CXCL1 and CXCL2, as well as IL-1ß, were higher in the colon of mice with antibiotic-induced dysbiosis. Neutrophils from antibiotic pre-treated mice had diminished surface expression of the chemokine receptor CXCR2, potentially explaining their inability to migrate to the site of infection. Blockade of CXCR2 increased susceptibility of control non-antibiotic treated mice to amebiasis. In conclusion, dysbiosis increased the severity of amebic colitis due to decreased neutrophil recruitment to the gut, which was due in part to decreased surface expression on neutrophils of CXCR2.
[Mh] Termos MeSH primário: Disenteria Amebiana/microbiologia
Microbiota/imunologia
Infiltração de Neutrófilos/imunologia
[Mh] Termos MeSH secundário: Animais
Pré-Escolar
Modelos Animais de Doenças
Disenteria Amebiana/imunologia
Entamoeba histolytica
Fezes/microbiologia
Citometria de Fluxo
Seres Humanos
Lactente
Camundongos
Camundongos Endogâmicos C57BL
Reação em Cadeia da Polimerase em Tempo Real
Receptores de Interleucina-8B/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Interleukin-8B)
[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:170818
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006513


  8 / 1257 MEDLINE  
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[PMID]:28763485
[Au] Autor:Jee J; Mourya R; Shivakumar P; Fei L; Wagner M; Bezerra JA
[Ad] Endereço:Divisions of Gastroenterology, Hepatology and Nutrition, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, United States of America.
[Ti] Título:Cxcr2 signaling and the microbiome suppress inflammation, bile duct injury, and the phenotype of experimental biliary atresia.
[So] Source:PLoS One;12(8):e0182089, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Biliary atresia is progressive fibro-inflammatory cholangiopathy of young children. Central to pathogenic mechanisms of injury is the tissue targeting by the innate and adaptive immune cells. Among these cells, neutrophils and the IL-8/Cxcl-8 signaling via its Cxcr2 receptor have been linked to bile duct injury. Here, we aimed to investigate whether the intestinal microbiome modulates Cxcr2-dependent bile duct injury and obstruction. Adult wild-type (WT) and Cxcr2-/- mice were fed a diet supplemented with sulfamethoxazole/trimethoprim (SMZ/TMP) during pregnancy and lactation, and their pups were injected intraperitoneally with rhesus rotavirus (RRV) within 24 hours of life to induce experimental biliary atresia. The maternal exposure to SMZ/TMP significantly lowered the incidence of jaundice and bile duct obstruction and resulted in improved survival, especially in Cxcr2-/- mice. Analyses of the microbiome by deep sequencing of 16S rRNA of the neonatal colon showed a delay in bacterial colonization of WT mice induced by SMZ/TMP, with a notable switch from Proteobacteria to Firmicutes. Interestingly, the genetic inactivation of Cxcr2 alone produced a similar bacterial shift. When treated with SMZ/TMP, Cxcr2-/- mice infected with RRV to induce experimental biliary atresia showed further enrichment of Corynebacterium, Anaerococcus and Streptococcus. Among these, Anaerococcus lactolyticus was significantly associated with a suppression of biliary injury, cholestasis, and survivability. These results suggest that the postnatal development of the intestinal microbiota is an important susceptibility factor for experimental biliary atresia.
[Mh] Termos MeSH primário: Ductos Biliares/lesões
Atresia Biliar/metabolismo
Inflamação/metabolismo
Microbiota
Receptores de Interleucina-8B/metabolismo
[Mh] Termos MeSH secundário: Animais
Atresia Biliar/microbiologia
Modelos Animais de Doenças
Feminino
Perfilação da Expressão Gênica
Lactação
Modelos Lineares
Macaca mulatta
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Fenótipo
Reação em Cadeia da Polimerase
Gravidez
Prenhez
RNA Ribossômico 16S/genética
Receptores de Interleucina-8B/genética
Rotavirus
Transdução de Sinais
Sulfametoxazol/administração & dosagem
Trimetoprima/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Ribosomal, 16S); 0 (Receptors, Interleukin-8B); AN164J8Y0X (Trimethoprim); JE42381TNV (Sulfamethoxazole)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182089


  9 / 1257 MEDLINE  
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[PMID]:28739876
[Au] Autor:Boro M; Balaji KN
[Ad] Endereço:Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore 560012, India.
[Ti] Título:CXCL1 and CXCL2 Regulate NLRP3 Inflammasome Activation via G-Protein-Coupled Receptor CXCR2.
[So] Source:J Immunol;199(5):1660-1671, 2017 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammation is an extensively concerted process that confers protection to the host encountering immune insult. The major inflammatory mediators include IL-1 family members, such as IL-1ß, and the functional activation of such molecules is arbitrated by their regulated cleavage brought about by components of a multiprotein complex called inflammasome. In this context, NLR family pyrin domain containing 3 (NLRP3) inflammasome activation often acts as a rate-limiting step in regulating critical cell-fate decisions in various inflammatory scenarios. In this study, we identify the G-protein-coupled receptor CXCR2 (recognizing chemokines CXCL1 and CXCL2) as another arm feeding into the regulated activation of NLRP3 inflammasome in macrophages. We demonstrate that in vivo blocking of CXCL1 and CXCL2 can significantly reduce the -induced bioactive IL-1ß production. Further, CXCL1 could amplify the inflammasome activation in in vivo mouse models of carrageenan-induced inflammation in footpads and air pouches. The mechanistic insights revealed CXCR2-driven protein kinase C µ-dependent integrin-linked kinase to be essential for CXCL1-mediated activation of NLRP3 inflammasome. Blocking the activity of integrin-linked kinase or protein kinase C µ either by small interfering RNA-mediated knockdown or pharmacological inhibitor compromised inflammasome activation and subsequent production of bioactive IL-1ß. Taken together, our study demonstrates CXCR2-driven activation of NLRP3 inflammasome in macrophages and indicates a potential host-directed therapeutic target to limit the damaging inflammation associated with overt production of proinflammatory IL-1ß.
[Mh] Termos MeSH primário: Inflamassomos/metabolismo
Macrófagos/imunologia
Mycobacterium tuberculosis/imunologia
Receptores Acoplados a Proteínas-G/metabolismo
Receptores de Interleucina-8B/metabolismo
Tuberculose/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Neutralizantes/administração & dosagem
Células Cultivadas
Quimiocina CXCL1/imunologia
Quimiocina CXCL1/metabolismo
Quimiocina CXCL2/imunologia
Quimiocina CXCL2/metabolismo
Seres Humanos
Interleucina-1beta/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Proteína 3 que Contém Domínio de Pirina da Família NLR/genética
Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo
RNA Interferente Pequeno/genética
Receptores Acoplados a Proteínas-G/imunologia
Receptores de Interleucina-8B/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (Chemokine CXCL1); 0 (Chemokine CXCL2); 0 (Cxcl1 protein, mouse); 0 (Cxcl2 protein, mouse); 0 (Inflammasomes); 0 (Interleukin-1beta); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (Nlrp3 protein, mouse); 0 (RNA, Small Interfering); 0 (Receptors, G-Protein-Coupled); 0 (Receptors, Interleukin-8B)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700129


  10 / 1257 MEDLINE  
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Texto completo
[PMID]:28705839
[Au] Autor:Gloude NJ; Khandelwal P; Luebbering N; Lounder DT; Jodele S; Alder MN; Lane A; Wilkey A; Lake KE; Litts B; Davies SM
[Ad] Endereço:Division of Bone Marrow Transplantation and Immune Deficiency and.
[Ti] Título:Circulating dsDNA, endothelial injury, and complement activation in thrombotic microangiopathy and GVHD.
[So] Source:Blood;130(10):1259-1266, 2017 Sep 07.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transplant-associated thrombotic microangiopathy (TA-TMA) is a common and poorly recognized complication of hematopoietic stem cell transplantation (HSCT) associated with excessive complement activation, likely triggered by endothelial injury. An important missing piece is the link between endothelial injury and complement activation. We hypothesized that neutrophil extracellular traps (NETs) mechanistically link endothelial damage with complement activation and subsequent TA-TMA. Neutrophil activation releases granule proteins together with double-stranded DNA (dsDNA) to form extracellular fibers known as NETs. NETs have been shown to activate complement and can be assessed in humans by quantification of dsDNA in serum. We measured levels of dsDNA, as a surrogate for NETs in 103 consecutive pediatric allogeneic transplant recipients at day 0, +14, +30, +60, and +100. A spike in dsDNA production around day +14 during engraftment was associated with subsequent TA-TMA development. Peak dsDNA production around day +14 was associated with interleukin-8-driven neutrophil recovery. Increased dsDNA levels at days +30, +60, and +100 were also associated with increased mortality and gastrointestinal graft-versus-host disease (GVHD). NETs may serve as a mechanistic link between endothelial injury and complement activation. NET formation may be one mechanism contributing to the clinical overlap between GVHD and TA-TMA.
[Mh] Termos MeSH primário: Ativação do Complemento/imunologia
DNA/sangue
Células Endoteliais/patologia
Doença Enxerto-Hospedeiro/sangue
Doença Enxerto-Hospedeiro/imunologia
Microangiopatias Trombóticas/sangue
Microangiopatias Trombóticas/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Criança
Pré-Escolar
Demografia
Armadilhas Extracelulares/metabolismo
Doença Enxerto-Hospedeiro/etiologia
Doença Enxerto-Hospedeiro/patologia
Transplante de Células-Tronco Hematopoéticas/efeitos adversos
Seres Humanos
Lactente
Interleucina-8/metabolismo
Estudos Longitudinais
Neutrófilos/metabolismo
Receptores de Interleucina-8A/metabolismo
Receptores de Interleucina-8B/metabolismo
Microangiopatias Trombóticas/etiologia
Microangiopatias Trombóticas/terapia
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-8); 0 (Receptors, Interleukin-8A); 0 (Receptors, Interleukin-8B); 9007-49-2 (DNA)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-05-782870



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