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[PMID]:29320816
[Au] Autor:Ismail HAHA; Kang BH; Kim JS; Lee JH; Choi IW; Cha GH; Yuk JM; Lee YH
[Ad] Endereço:Department of Infection Biology, Chungnam National University School of Medicine, Daejeon 34134, Korea.
[Ti] Título:IL-12 and IL-23 Production in Toxoplasma gondii- or LPS-Treated Jurkat T Cells via PI3K and MAPK Signaling Pathways.
[So] Source:Korean J Parasitol;55(6):613-622, 2017 Dec.
[Is] ISSN:1738-0006
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:IL-12 and IL-23 are closely related in structure, and have been shown to play crucial roles in regulation of immune responses. However, little is known about the regulation of these cytokines in T cells. Here, we investigated the roles of PI3K and MAPK pathways in IL-12 and IL-23 production in human Jurkat T cells in response to Toxoplasma gondii and LPS. IL-12 and IL-23 production was significantly increased in T cells after stimulation with T. gondii or LPS. T. gondii and LPS increased the phosphorylation of AKT, ERK1/2, p38 MAPK, and JNK1/2 in T cells from 10 min post-stimulation, and peaked at 30-60 min. Inhibition of the PI3K pathway reduced IL-12 and IL-23 production in T. gondii-infected cells, but increased in LPS-stimulated cells. IL-12 and IL-23 production was significantly reduced by ERK1/2 and p38 MAPK inhibitors in T. gondii- and LPS-stimulated cells, but not in cells treated with a JNK1/2 inhibitor. Collectively, IL-12 and IL-23 production was positively regulated by PI3K and JNK1/2 in T. gondii-infected Jurkat cells, but negatively regulated in LPS-stimulated cells. And ERK1/2 and p38 MAPK positively regulated IL-12 and IL-23 production in Jurkat T cells. These data indicate that T. gondii and LPS induced IL-12 and IL-23 production in Jurkat T cells through the regulation of the PI3K and MAPK pathways; however, the mechanism underlying the stimulation of IL-12 and IL-23 production by T. gondii in Jurkat T cells is different from that of LPS.
[Mh] Termos MeSH primário: Interleucina-12/metabolismo
Interleucina-23/metabolismo
Lipopolissacarídeos/imunologia
Sistema de Sinalização das MAP Quinases/imunologia
Sistema de Sinalização das MAP Quinases/fisiologia
Fosfatidilinositol 3-Quinases/imunologia
Fosfatidilinositol 3-Quinases/fisiologia
Toxoplasma/imunologia
[Mh] Termos MeSH secundário: Células Cultivadas
Seres Humanos
Células Jurkat
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/fisiologia
Proteína Quinase 8 Ativada por Mitógeno/metabolismo
Proteína Quinase 8 Ativada por Mitógeno/fisiologia
Proteína Quinase 9 Ativada por Mitógeno/metabolismo
Proteína Quinase 9 Ativada por Mitógeno/fisiologia
Fosforilação
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-23); 0 (Lipopolysaccharides); 187348-17-0 (Interleukin-12); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.1.24 (Mitogen-Activated Protein Kinase 9); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 8); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.3347/kjp.2017.55.6.613


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[PMID]:29441964
[Au] Autor:Kono Y; Miyoshi S; Fujita T
[Ti] Título:Dextran sodium sulfate alters cytokine production in macrophages .
[So] Source:Pharmazie;71(11):619-624, 2016 Nov 02.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Macrophages have been assumed to have a crucial role in the development of inflammatory bowel disease (IBD). However, involvement of intestinal macrophages in IBD onset and functional alterations of macrophages during IBD development has not been clarified. We investigated the effect of exposure of compounds used in the induction of colitis in mice on the immune responses of peritoneal macrophages in mice. 2,4,6- trinitrobenzenesulfonic acid and oxazolone did not affect the production of interleukin (IL)-10 and IL-12 from lipopolysaccharide (LPS)-stimulated peritoneal macrophages from BALB/c mice. A significant increase in IL-10 secretion and decrease in IL-12 production from LPS-stimulated macrophages were observed upon exposure to dextran sodium sulfate (DSS). TNF-α production was enhanced significantly by exposure to DSS and LPS. The level of nitric-oxide production from macrophages was increased slightly by exposure to DSS and LPS. Expression of sphingosine kinase-1 and LIGHT (both of which are specific biomarkers of M2b macrophages) was observed in macrophages upon DSS exposure. Alteration of cytokine production in macrophages was observed upon DSS exposure in the absence of LPS stimulation. Peritoneal macrophages from C57BL/6 mice showed similar responses to peritoneal macrophages from BALB/c mice against DSS. These results suggest that DSS directs the immune response of macrophages towards the M2b phenotype.
[Mh] Termos MeSH primário: Citocinas/biossíntese
Sulfato de Dextrana/farmacologia
Macrófagos Peritoneais/metabolismo
[Mh] Termos MeSH secundário: Animais
Colite/induzido quimicamente
Colite/patologia
Feminino
Técnicas In Vitro
Interleucina-10/biossíntese
Interleucina-10/genética
Interleucina-12/biossíntese
Interleucina-12/genética
Lipopolissacarídeos/farmacologia
Macrófagos Peritoneais/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Óxido Nítrico/biossíntese
Fosfotransferases (Aceptor do Grupo Álcool)/biossíntese
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Especificidade da Espécie
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/biossíntese
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (IL10 protein, mouse); 0 (Lipopolysaccharides); 0 (Tnfsf14 protein, mouse); 0 (Tumor Necrosis Factor Ligand Superfamily Member 14); 130068-27-8 (Interleukin-10); 187348-17-0 (Interleukin-12); 31C4KY9ESH (Nitric Oxide); 9042-14-2 (Dextran Sulfate); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.- (sphingosine kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6688


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[PMID]:28463694
[Au] Autor:Liu L; Yi H; He H; Pan H; Cai L; Ma Y
[Ad] Endereço:Key Lab of Health Informatics of Chinese Academy of Sciences, Guangdong Key Laboratory of Nanomedicine, Shenzhen Institutes of Advanced Technology, Chinese Academy of Science, Shenzhen 518055, PR China.
[Ti] Título:Tumor associated macrophage-targeted microRNA delivery with dual-responsive polypeptide nanovectors for anti-cancer therapy.
[So] Source:Biomaterials;134:166-179, 2017 Jul.
[Is] ISSN:1878-5905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Repolarizing Tumor-associated macrophages (TAMs) to anti-tumor M1 macrophages with microRNA (miR) is a plausible approach for cancer treatment. However, how to achieve TAM-targeted miR delivery remains a challenge. The present study generated redox/pH dual-responsive hybrid polypeptide nanovectors, which consisted of self-crosslinked redox-responsive nanoparticles based on galactose-functionalized n-butylamine-poly(l-lysine)-b-poly(l-cysteine) polypeptides (GLC) coated with DCA-grafted sheddable PEG-PLL (sPEG) copolymers. The ex vivo study showed that sPEG shielded cationic GLC core at physiological pH but quickly shed off to re-expose GLC due to it charge reversible property. Encapsulation with sPEG/GLC nanovectors effectively facilitated macrophage-targeted miR delivery at the acidic condition but diminished miR uptake at neutral pH. Administration of miR155-loaded sPEG/GLC (sPEG/GLC/155) nanocomplexes increased miR155 expression in TAMs about 100-400 folds both in vitro and in vivo. sPEG/GLC/155 also effectively repolarized immunosuppressive TAMs to anti-tumor M1 macrophages through elevating M1 macrophage markers (IL-12, iNOS, MHC II) and suppressing M2 macrophage markers (Msr2 and Arg1) in TAMs. Moreover, the treatment of sPEG/GLC/155 significantly increased activated T lymphocytes and NK cells in tumors, which consequently led to robust tumor regression. Hence, TAM-targeted delivery of miR with redox/pH dual-responsive sPEG/GLC nanovectors could be a promising approach to re-polarize TAMs to M1 macrophages in situ and induce tumor regression.
[Mh] Termos MeSH primário: MicroRNAs/genética
Nanopartículas/química
Peptídeos/química
[Mh] Termos MeSH secundário: Animais
Eletroforese em Gel de Ágar
Feminino
Interleucina-12/metabolismo
Células Matadoras Naturais/metabolismo
Espectroscopia de Ressonância Magnética
Melanoma/metabolismo
Melanoma/terapia
Melanoma Experimental
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Nus
MicroRNAs/fisiologia
Óxido Nítrico Sintase Tipo II/metabolismo
Células RAW 264.7
Transdução de Sinais/genética
Transdução de Sinais/fisiologia
Linfócitos T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs); 0 (Peptides); 187348-17-0 (Interleukin-12); EC 1.14.13.39 (Nitric Oxide Synthase Type II)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:29320562
[Au] Autor:Jarosz-Biej M; Kaminska N; Matuszczak S; Cichon T; Pamula-Pilat J; Czapla J; Smolarczyk R; Skwarzynska D; Kulik K; Szala S
[Ad] Endereço:Center for Translational Research and Molecular Biology of Cancer, Maria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Gliwice Branch, Gliwice, Poland.
[Ti] Título:M1-like macrophages change tumor blood vessels and microenvironment in murine melanoma.
[So] Source:PLoS One;13(1):e0191012, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumor-associated macrophages (TAMs) play a significant role in at least two key processes underlying neoplastic progression: angiogenesis and immune surveillance. TAMs phenotypic changes play important role in tumor vessel abnormalization/ normalization. M2-like TAMs stimulate immunosuppression and formation of defective tumor blood vessels leading to tumor progression. In contrast M1-like TAMs trigger immune response and normalize irregular tumor vascular network which should sensitize cancer cells to chemo- and radiotherapy and lead to tumor growth regression. Here, we demonstrated that combination of endoglin-based DNA vaccine with interleukin 12 repolarizes TAMs from tumor growth-promoting M2-like phenotype to tumor growth-inhibiting M1-like phenotype. Combined therapy enhances tumor infiltration by CD4+, CD8+ lymphocytes and NK cells. Depletion of TAMs as well as CD8+ lymphocytes and NK cells, but not CD4+ lymphocytes, reduces the effect of combined therapy. Furthermore, combined therapy improves tumor vessel maturation, perfusion and reduces hypoxia. It caused that suboptimal doses of doxorubicin reduced the growth of tumors in mice treated with combined therapy. To summarize, combination of antiangiogenic drug and immunostimulatory agent repolarizes TAMs phenotype from M2-like (pro-tumor) into M1-like (anti-tumor) which affects the structure of tumor blood vessels, improves the effect of chemotherapy and leads to tumor growth regression.
[Mh] Termos MeSH primário: Interleucina-12/administração & dosagem
Macrófagos/fisiologia
Melanoma Experimental/irrigação sanguínea
Melanoma Experimental/imunologia
Neovascularização Patológica/patologia
Microambiente Tumoral/imunologia
[Mh] Termos MeSH secundário: Inibidores da Angiogênese/administração & dosagem
Animais
Antibióticos Antineoplásicos/farmacologia
Linfócitos T CD4-Positivos/efeitos dos fármacos
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/efeitos dos fármacos
Linfócitos T CD8-Positivos/imunologia
Proliferação Celular/efeitos dos fármacos
Doxorrubicina/farmacologia
Feminino
Células Matadoras Naturais/efeitos dos fármacos
Células Matadoras Naturais/imunologia
Macrófagos/efeitos dos fármacos
Melanoma Experimental/tratamento farmacológico
Melanoma Experimental/patologia
Camundongos
Camundongos Endogâmicos C57BL
Neovascularização Patológica/tratamento farmacológico
Neovascularização Patológica/imunologia
Células Tumorais Cultivadas
Vacinas de DNA/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Antibiotics, Antineoplastic); 0 (Vaccines, DNA); 187348-17-0 (Interleukin-12); 80168379AG (Doxorubicin)
[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:180111
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191012


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[PMID]:29381995
[Au] Autor:Yan Y; Wang J; Qu B; Zhang Y; Wei Y; Liu H; Wu C
[Ad] Endereço:Department of Neurology.
[Ti] Título:CXCL13 and TH1/Th2 cytokines in the serum and cerebrospinal fluid of neurosyphilis patients.
[So] Source:Medicine (Baltimore);96(47):e8850, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neurosyphilis is a chronic infectious disease with involvement of central nervous system infection by Treponema pallidum. This study was to investigate the contents of B lymphocyte chemokine 1 (BLC-1/chemokine [C-X-C motif] ligand 13), Th1 cytokines (Interleukin [IL]-2, IL-12, and Interferon [IFN]-γ), and Th2 cytokines (IL-6 and IL-10) in serum and cerebrospinal fluid (CSF) of HIV-negative patients with neurosyphilis before and after treatment, aiming to elucidate roles of CXCL13 and Th1/Th2 cytokines in immune response to and pathogenesis of neurosyphilis.Enzyme-linked immunosorbent assay was employed to detect the contents of CXCL13, IL-2, IL-12, IFN-γ, IL-6, and IL-10 in serum and CSF of 47 HIV-negative patients with neurosyphilis, 36 syphilis patients without neurological involvement and 23 controls (noninfectious intracranial disease) before, 3 and 12 months after treatment with high dose penicillin.Results showed that there was no significant difference in blood CXCL13 content among 3 groups (P > .05); CSF CXCL13 content in neurosyphilis patients was significantly higher than in other 2 groups (P < .001), and positively related to leucocyte count, protein concentration, and IgG index. IL-6 and IL-10 contents of the serum and CSF in neurosyphilis patients were markedly higher than in other 2 groups (P < .05 or .01), but IL-2, IL-12, and IFN-γ of the serum and CSF were significantly lower than in other 2 groups (P < .05 or .01). The IL-6, IL-10, IL-2, IL-12, and IFN-γ contents of the serum and CSF were comparable between control group and syphilis group (P > .05). CSF CXCL13 content was positively related with IL-6 and IL-10 content, while negatively related to IL-12 content in neurosyphilis patients. CSF IL-6 content was negatively related with IL-12 content. In neurosyphilis patients, the CSF CXCL13 content reduced significantly at 3 and 12 months (P < .001), the CSF IL-2 and IL-12 contents increased significantly at 12 months, and CSF IL-6 contents reduced significantly at 12 months after treatment (P < .05 or .01).It is concluded that neurosyphilis patients did not have normal immune function. CXCL13 and Th1/Th2 cytokines are involved in the immune response of neurosyphilis patients. CSF CXCL13 and Th1/Th2 cytokines contents may be used for the diagnosis and evaluation of therapeutic efficacy of neurosyphilis.
[Mh] Termos MeSH primário: Quimiocina CXCL13/análise
Citocinas/análise
Neurossífilis/sangue
Neurossífilis/líquido cefalorraquidiano
[Mh] Termos MeSH secundário: Adulto
Idoso
Antibacterianos/uso terapêutico
Estudos de Casos e Controles
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Interferon gama/análise
Interleucina-10/análise
Interleucina-12/análise
Interleucina-2/análise
Interleucina-6/análise
Masculino
Meia-Idade
Neurossífilis/tratamento farmacológico
Penicilinas/uso terapêutico
Sífilis/sangue
Sífilis/líquido cefalorraquidiano
Sífilis/tratamento farmacológico
Equilíbrio Th1-Th2/efeitos dos fármacos
Adulto Jovem
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (CXCL13 protein, human); 0 (Chemokine CXCL13); 0 (Cytokines); 0 (IL10 protein, human); 0 (IL2 protein, human); 0 (IL6 protein, human); 0 (Interleukin-2); 0 (Interleukin-6); 0 (Penicillins); 130068-27-8 (Interleukin-10); 187348-17-0 (Interleukin-12); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008850


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[PMID]:29248447
[Au] Autor:Echeverría S; Leiguez E; Guijas C; do Nascimento NG; Acosta O; Teixeira C; Leiva LC; Rodríguez JP
[Ad] Endereço:Laboratorio de Investigación en Proteínas, Instituto de Química Básica y Aplicada del Nordeste Argentino (UNNE - CONICET), Argentina.
[Ti] Título:Evaluation of pro-inflammatory events induced by Bothrops alternatus snake venom.
[So] Source:Chem Biol Interact;281:24-31, 2018 Feb 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Inflammation is a major local feature of envenomation by bothropic snakes being characterized by a prominent local edema, pain, and extensive swelling. There are reports demonstrating that whole Bothrops snake venoms and toxins isolated from them are able to activate macrophages functions, such as phagocytosis, production of reactive oxygen, cytokines and eicosanoids, however, little is known about the effects of Bothrops alternatus (B.a.) venom on macrophages. In this work, we evaluated the proinflammatory effects of B.a. venom with in vivo and in vitro experiments using the Raw 264.7 cell line and mouse peritoneal macrophages. We detected that B.a. venom augments cell permeability (2-fold), and cellular extravasation (mainly neutrophils), increase proinflammatory cytokines IL1 (∼300-fold), IL12 (∼200-fold), and TNFα (∼80-fold) liberation and induce the expression of enzymes related to lipid signaling, such as cPLA and COX-2. Additionally, using lipidomic techniques we detected that this venom produces a release of arachidonic acid (∼10 nMol/mg. Protein) and other fatty acids (16:0 and 18:1 n-9c). Although much of these findings were described in inflammatory processes induced by other bothropic venoms, here we demonstrate that B.a. venom also stimulates pro-inflammatory pathways involving lipid mediators of cell signaling. In this sense, lipidomics analysis of macrophages stimulated with B.a. venom evidenced that the main free fatty acids are implicated in the inflammatory response, and also demonstrated that this venom, is able to activate lipid metabolism even with a low content of PLA .
[Mh] Termos MeSH primário: Bothrops/metabolismo
Macrófagos Peritoneais/efeitos dos fármacos
Venenos de Serpentes/toxicidade
[Mh] Termos MeSH secundário: Animais
Ácido Araquidônico/análise
Ácido Araquidônico/metabolismo
Permeabilidade da Membrana Celular/efeitos dos fármacos
Células Cultivadas
Ciclo-Oxigenase 2/metabolismo
Citocinas/metabolismo
Edema/etiologia
Ácidos Graxos/análise
Ácidos Graxos/metabolismo
Cromatografia Gasosa-Espectrometria de Massas
Fosfolipases A2 do Grupo IV/metabolismo
Interleucina-1/metabolismo
Interleucina-12/metabolismo
Macrófagos Peritoneais/citologia
Macrófagos Peritoneais/metabolismo
Masculino
Camundongos
Neutrófilos/efeitos dos fármacos
Neutrófilos/imunologia
Neutrófilos/metabolismo
Células RAW 264.7
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Fatty Acids); 0 (Interleukin-1); 0 (Snake Venoms); 0 (Tumor Necrosis Factor-alpha); 187348-17-0 (Interleukin-12); 27YG812J1I (Arachidonic Acid); EC 1.14.99.1 (Cyclooxygenase 2); EC 3.1.1.4 (Group IV Phospholipases A2)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171218
[St] Status:MEDLINE


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[PMID]:28747343
[Au] Autor:Savage AK; Liang HE; Locksley RM
[Ad] Endereço:Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94158.
[Ti] Título:The Development of Steady-State Activation Hubs between Adult LTi ILC3s and Primed Macrophages in Small Intestine.
[So] Source:J Immunol;199(5):1912-1922, 2017 09 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Group 3 innate lymphoid cells (ILC3s) are important for intestinal health, particularly in controlling inflammation in response to epithelial dysregulation, but their role during homeostasis remains less well understood. We generated IL-22 reporter mice to assess production of this key cytokine by ILC3s in the small intestine during development and under basal conditions. Although IL-22 is produced by a variety of lymphocyte populations, constitutively high IL-22 expression was limited to lymphoid-tissue inducer (LTi) cells residing in lymph node-like structures in the gut called solitary intestinal lymphoid tissues (SILT). Constitutive IL-22 expression was dependent on the microbiota and MyD88 signaling, appeared upon weaning, and was present across the spectrum of SILT, including in cryptopatches. Activated SILT LTi cells colocalized with a rare subpopulation of activated macrophages constitutively positive for IL-12/23 p40 and capable of activating neonatal LTi cells in response to TLR stimulus. Thus, weaning leads to the organization of innate immune activation hubs at SILT that mature and are continuously sustained by signals from the microbiota. This functional and anatomic organization constitutes a significant portion of the steady-state IL-23/IL-22 axis.
[Mh] Termos MeSH primário: Interleucinas/metabolismo
Intestino Delgado/imunologia
Linfócitos/imunologia
Macrófagos/imunologia
Estruturas Linfoides Terciárias/imunologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Células Cultivadas
Imunidade Inata
Interleucina-12/metabolismo
Interleucina-23/metabolismo
Interleucinas/genética
Intestino Delgado/anatomia & histologia
Ativação Linfocitária
Linfócitos/citologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Microbiota/imunologia
Fator 88 de Diferenciação Mieloide/metabolismo
Transdução de Sinais
Estruturas Linfoides Terciárias/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-23); 0 (Interleukins); 0 (Myd88 protein, mouse); 0 (Myeloid Differentiation Factor 88); 0 (interleukin-22); 187348-17-0 (Interleukin-12)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700155


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Chiari, Egler
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[PMID]:29176759
[Au] Autor:Magalhães LMD; Viana A; de Jesus AC; Chiari E; Galvão L; Gomes JA; Gollob KJ; Dutra WO
[Ad] Endereço:Laboratório de Biologia das Interações Celulares, Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
[Ti] Título:Distinct Trypanosoma cruzi isolates induce activation and apoptosis of human neutrophils.
[So] Source:PLoS One;12(11):e0188083, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neutrophils are critical players in the first line of defense against pathogens and in the activation of subsequent cellular responses. We aimed to determine the effects of the interaction of Trypanosoma cruzi with human neutrophils, using isolates of the two major discrete type units (DTUs) associated with Chagas' disease in Latin America (clone Col1.7G2 and Y strain, DTU I and II, respectively). Thus, we used CFSE-stained trypomastigotes to measure neutrophil-T. cruzi interaction, neutrophil activation, cytokine expression and death, after infection with Col1.7G2 and Y strain. Our results show that the frequency of CFSE+ neutrophils, indicative of interaction, and CFSE intensity on a cell-per-cell basis were similar when comparing Col1.7G2 and Y strains. Interaction with T. cruzi increased neutrophil activation, as measured by CD282, CD284, TNF and IL-12 expression, although at different levels between the two strains. No change in IL-10 expression was observed after interaction of neutrophils with either strain. We observed that exposure to Y and Col1.7G2 caused marked neutrophil death. This was specific to neutrophils, since interaction of either strain with monocytes did not cause death. Our further analysis showed that neutrophil death was a result of apoptosis, which was associated with an upregulation of TNF-receptor, TNF and FasLigand, but not of Fas. Induction of TNF-associated neutrophil apoptosis by the different T. cruzi isolates may act as an effective common mechanism to decrease the host's immune response and favor parasite survival.
[Mh] Termos MeSH primário: Apoptose
Ativação de Neutrófilo
Neutrófilos/citologia
Trypanosoma cruzi/isolamento & purificação
[Mh] Termos MeSH secundário: Adulto
Antígenos CD/metabolismo
Sobrevivência Celular
Proteína Ligante Fas/metabolismo
Fluoresceínas/metabolismo
Seres Humanos
Interleucina-10/metabolismo
Interleucina-12/metabolismo
Neutrófilos/metabolismo
Receptores do Fator de Necrose Tumoral/metabolismo
Succinimidas/metabolismo
Receptor 2 Toll-Like/metabolismo
Receptor 4 Toll-Like/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
Adulto Jovem
Receptor fas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5-(6)-carboxyfluorescein diacetate succinimidyl ester); 0 (Antigens, CD); 0 (FAS protein, human); 0 (Fas Ligand Protein); 0 (Fluoresceins); 0 (Receptors, Tumor Necrosis Factor); 0 (Succinimides); 0 (Toll-Like Receptor 2); 0 (Toll-Like Receptor 4); 0 (Tumor Necrosis Factor-alpha); 0 (fas Receptor); 130068-27-8 (Interleukin-10); 187348-17-0 (Interleukin-12)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188083


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[PMID]:29023599
[Au] Autor:Lee YK; Landuyt AE; Lobionda S; Sittipo P; Zhao Q; Maynard CL
[Ad] Endereço:Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, United States of America.
[Ti] Título:TCR-independent functions of Th17 cells mediated by the synergistic actions of cytokines of the IL-12 and IL-1 families.
[So] Source:PLoS One;12(10):e0186351, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The development of Th17 cells is accompanied by the acquisition of responsiveness to both IL-12 and IL-23, cytokines with established roles in the development and/or function of Th1 and Th17 cells, respectively. IL-12 signaling promotes antigen-dependent Th1 differentiation but, in combination with IL-18, allows the antigen-independent perpetuation of Th1 responses. On the other hand, while IL-23 is dispensable for initial commitment to the Th17 lineage, it promotes the pathogenic function of the Th17 cells. In this study, we have examined the overlap between Th1 and Th17 cells in their responsiveness to common pro-inflammatory cytokines and how this affects the antigen-independent cytokine responses of Th17 cells. We found that in addition to the IL-1 receptor, developing Th17 cells also up-regulate the IL-18 receptor. Consequently, in the presence of IL-1ß or IL-18, and in the absence of TCR activation, Th17 cells produce Th17 lineage cytokines in a STAT3-dependent manner when stimulated with IL-23, and IFN© via a STAT4-dependent mechanism when stimulated with IL-12. Thus, building on previous findings of antigen-induced plasticity of Th17 cells, our results indicate that this potential of Th17 cells extends to their cytokine-dependent antigen-independent responses. Collectively, our data suggest a model whereby signaling via either IL-1ß or IL-18 allows for bystander responses of Th17 cells to pathogens or pathogen products that differentially activate innate cell production of IL-12 or IL-23.
[Mh] Termos MeSH primário: Interleucina-12/metabolismo
Interleucina-1/metabolismo
Receptores de Antígenos de Linfócitos T/metabolismo
Células Th17/metabolismo
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD4-Positivos/citologia
Diferenciação Celular/efeitos dos fármacos
Células Cultivadas
Interleucina-1beta/metabolismo
Interleucina-6/farmacologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Interferência de RNA
Receptores de Antígenos de Linfócitos T/genética
Fator de Transcrição STAT3/antagonistas & inibidores
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais/efeitos dos fármacos
Células Th1/citologia
Células Th1/imunologia
Células Th1/metabolismo
Células Th17/citologia
Células Th17/efeitos dos fármacos
Fator de Crescimento Transformador beta/farmacologia
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Receptors, Antigen, T-Cell); 0 (STAT3 Transcription Factor); 0 (Transforming Growth Factor beta); 187348-17-0 (Interleukin-12)
[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:171013
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186351


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[PMID]:28974421
[Au] Autor:Nakashima A; Suzuki K; Asayama Y; Konno M; Saito K; Yamazaki N; Takimoto H
[Ad] Endereço:euglena Co., Ltd., 5-33-1 Shiba, Minato-ku, Tokyo, 108-0014, Japan.
[Ti] Título:Oral administration of Euglena gracilis Z and its carbohydrate storage substance provides survival protection against influenza virus infection in mice.
[So] Source:Biochem Biophys Res Commun;494(1-2):379-383, 2017 Dec 09.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Euglena gracilis Z is a micro-algae that is used as a food or nutritional supplement. Paramylon, the carbohydrate storage substance of Euglena gracilis Z has ß-1, 3-glucan structure. Euglena gracilis Z and paramylon are reported to affect the immune system. In this study, we investigated the protective effects of Euglena gracilis Z and paramylon against influenza virus infection in mice. Euglena gracilis Z and paramylon were administered to mice as a 2% dietary mixture ad libitum. At 2 weeks after initiation of dietary administration, mice were infected intranasally with influenza virus A/PR/8/34 (H1N1). Survival rate was monitored 10 days after infection. In addition, we performed virus titer and cytokine profiles in the lung. High survival rates were observed for Euglena gracilis Z and paramylon-treated groups compared to the control group. Significantly lower virus titer in the lung was observed in the Euglena gracilis Z and paramylon-treated groups compared to the control group from day 1 after infection. Higher amount of IL-1ß, IL-6, IL-12 (p70), IFN-γ, and IL-10 was observed in the paramylon groups compared to the control group. Our data therefore reveals a novel immunoregulatory role of the Euglena gracilis Z and paramylon which provides protection against influenza virus infection.
[Mh] Termos MeSH primário: Adjuvantes Imunológicos/administração & dosagem
Suplementos Nutricionais
Euglena gracilis/imunologia
Glucanos/administração & dosagem
Pulmão/efeitos dos fármacos
Infecções por Orthomyxoviridae/dietoterapia
[Mh] Termos MeSH secundário: Administração Oral
Animais
Euglena gracilis/química
Feminino
Vírus da Influenza A Subtipo H1N1/efeitos dos fármacos
Vírus da Influenza A Subtipo H1N1/crescimento & desenvolvimento
Vírus da Influenza A Subtipo H1N1/patogenicidade
Interferon gama/biossíntese
Interferon gama/imunologia
Interleucina-10/biossíntese
Interleucina-10/imunologia
Interleucina-12/biossíntese
Interleucina-12/imunologia
Interleucina-1beta/biossíntese
Interleucina-1beta/imunologia
Interleucina-6/biossíntese
Interleucina-6/imunologia
Pulmão/imunologia
Pulmão/virologia
Camundongos
Camundongos Endogâmicos BALB C
Infecções por Orthomyxoviridae/imunologia
Infecções por Orthomyxoviridae/mortalidade
Infecções por Orthomyxoviridae/virologia
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Glucans); 0 (IL10 protein, mouse); 0 (IL1B protein, mouse); 0 (Interleukin-1beta); 0 (Interleukin-6); 130068-27-8 (Interleukin-10); 187348-17-0 (Interleukin-12); 51052-65-4 (paramylon); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE



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