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Topical interleukin-1 receptor antagonist inhibits inflammatory cell infiltration into the cornea

STAPLETON, W. Michael; CHAURASIA, Shyam S.; MEDEIROS, Fabricio W.; MOHAN, Rajiv R.; SINHA, Sunilima; WILSON, Steven E.
Fonte: ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD Publicador: ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
Tipo: Artigo de Revista Científica
Português
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55.86%
Interleukin (IL)-1 alpha and beta are important modulators of many functions of corneal epithelial and stromal cells that occur following injury to the cornea, including the influx of bone marrow-derived inflammatory cells into the stroma attracted by chemokines released from the stroma and epithelium. In this study, we examined the effect of topical soluble IL-1 receptor antagonist on bone marrow-derived cell influx following corneal epithelial scrape injury in a mouse model. C57BL/6 mice underwent corneal epithelial scrape followed by application of IL-1 receptor antagonist (Amgen, Thousand Oaks, CA) at a concentration of 20 mg/ml or vehicle for 24 h prior to immunocytochemical detection of marker CD11b-positive cells into the stroma. In two experiments, topical IL-1 receptor antagonist had a marked effect in blocking cell influx. For example, in experiment 1, topical IL-1 receptor antagonist markedly reduced detectible CD11b-positive cells into the corneal stroma at 24 It after epithelial injury compared with the vehicle control (3.5 +/- 0.5 (standard error of the mean) cells/400x field and 13.9 +/- 1.2 cells/400x field, respectively, p < 0.01). A second experiment with a different observer performing cell counting had the same result. Thus...

An interleukin-1 beta (IL-1 beta) single-nucleotide polymorphism at position 3954 and red complex periodontopathogens independently and additively modulate the levels of IL-1 beta in diseased periodontal tissues

FERREIRA JR., Samuel B.; TROMBONE, Ana Paula F.; REPEKE, Carlos E.; CARDOSO, Cristina R.; MARTINS JR., Walter; SANTOS, Carlos F.; TREVILATTO, Paula Cristina; AVILA-CAMPOS, Mario J.; CAMPANELLI, Ana Paula; SILVA, Joao S.; GARLET, Gustavo P.
Fonte: AMER SOC MICROBIOLOGY Publicador: AMER SOC MICROBIOLOGY
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
55.86%
Inflammatory cytokines such as interieukin-1 beta (IL-1 beta) are involved in the pathogenesis of periodontal diseases. A high individual variation in the levels of IL-10 mRNA has been verified, which is possibly determined by genetic polymorphisms and/or by the presence of periodontopathogens such as Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, and Aggregatibacter actinomycetemcomitans. In this study, we investigated the role of an IL-10 promoter single-nucleotide polymorphism at position 3954 [IL-1 beta(3954) SNP] and the presence of the periodontopathogens in the determination of the IL-1 beta levels in the periodontal tissues of nonsmoking chronic periodontitis (CP) patients (n = 117) and control (C) subjects in = 175) and the possible correlations with the clinical parameters of the disease. IL-1 beta(3954) SNP was investigated by restriction fragment length polymorphism, while the IL-1 beta levels and the presence of the periodontopathogens were determined by real-time PCR. Similar frequencies of IL-1 beta(3954) SNP were found in the C and CP groups, in spite of a trend toward a higher incidence of T alleles in the CP group. The IL-1 beta (3954) SNP CT and TT genotypes, as well as P. gingivalis, T. forsythia...

Dor e qualidade de vida relacionada à saúde de pacientes com câncer: influência das citocinas pró-inflamatórias TNF-α, IL-6, IL-8 e IL -1β; Pain and health-related quality of life in patients with cancer: influence of pro-inflammatory cytokines TNF-α, IL-6, IL-8 e IL-1β

Ferreira, Karine Azevêdo São Leão
Fonte: Biblioteca Digitais de Teses e Dissertações da USP Publicador: Biblioteca Digitais de Teses e Dissertações da USP
Tipo: Tese de Doutorado Formato: application/pdf
Publicado em 13/02/2008 Português
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Objetivos: avaliar a associação entre dor oncológica crônica e as citocinas pró-inflamatórias interleucina-6 (IL-6), IL-8, IL-1β e TNF-α, e a interferência destas citocinas na relação entre dor, qualidade de vida relacionada à saúde (QVRS) e desempenho funcional (DF). Método: 220 pacientes ambulatoriais com câncer, que não haviam recebido nenhum tratamento antineoplásico nos últimos 30 dias, foram avaliados pelo Inventário Breve de Dor, Questionário de Dor McGill (MPQ), Inventário de Depressão de Beck, Escala de Desempenho Funcional de Karnofsky e a escala de QVRS, EORTC-QLQ-c30. Os níveis plasmáticos das citocinas foram dosados através do teste imunoenzimático ELISA e comparados entre pacientes com dor leve (G1), moderada a intensa (G2) e sem dor (G3) usando a ANOVA ou o teste de Kruskal-Wallis seguido por análise de múltiplas comparações. Os pacientes do G1 e G2 apresentavam apenas dor oncólogica e estavam em uso de analgésicos. Os do G3 tinham câncer, mas não apresentaram dor ou fizeram uso de analgésicos nos últimos 14 dias. 23 voluntários saudáveis (G4) foram incluídos como controle. A ANCOVA foi utilizada para avaliar o efeito das citocinas na relação dor, QVRS e DF. A análise de Árvore de Classificação e Regressão (CART) avaliou a relação entre citocinas e níveis de dor...

Mensuração sérica de Interleucina-1 β, Interleucina-6, Interleucina-10 e Fator de Necrose Tumoral α em cães com doença periodontal crônica; Measurement of serum Interleukin-1β, Interleukin-6, Interleukin 10 and Tumor Necrosis Factor-α in dogs with chronic periodontal disease

Cardoso, Juliana Kowalesky
Fonte: Biblioteca Digitais de Teses e Dissertações da USP Publicador: Biblioteca Digitais de Teses e Dissertações da USP
Tipo: Tese de Doutorado Formato: application/pdf
Publicado em 14/12/2012 Português
Relevância na Pesquisa
55.87%
A doença periodontal é resultado da inflamação das estruturas periodontais em resposta ao biofilme dentário presente na superfície dental e sulco gengival. Sua etiopatogenia é multifatorial e complexa. Na periodontite crônica há bacteremia freqüente durante rotinas diárias como escovação dentária e mastigação e acredita-se que esse estímulo constante ao sistema imunológico possa causar repercussões sistêmicas nos pacientes, como arterioescleroses. Uma das formas atuais de se mensurar essa alteração é pela presença de mediadores inflamatórios séricos. Sendo as proteínas de fase aguda, como as citocinas, as mais avaliadas. Assim como os trabalhos encontrados para a espécie humana, propôsse a mensuração sérica das interleucinas IL-1, IL-6, IL-10 e TNF-α em cães com doença periodontal crônica. Como grupo controle, utilizaram-se os mesmos pacientes após tratamento periodontal, mensurando as mesmas interleucinas depois de 21 dias do tratamento. Como resultado todas as interleucinas sofreram alteração, porém somente a IL-6 teve redução estatisticamente significativa após o tratamento periodontal. Todavia atenta-se para os elevados valores encontrados em alguns pacientes, o que pode demonstrar importante alteração sistêmica.; Periodontal disease is the result of inflammation of the periodontal structures in response to the biofilm present on the tooth surface and the gingival sulcus. Its pathogenesis is multifactorial and complex. Bacteremia in chronic periodontitis is constant during daily routines...

Macrophage Cell Activation with Acute Apical Abscess Contents Determined by Interleukin-1 Beta and Tumor Necrosis Factor Alpha Production

Sousa, Ezilmara L. R.; Martinho, Frederico C.; Leite, Fabio R. M.; Nascimento, Gustavo G.; Gomes, Brenda P. F. A.
Fonte: Elsevier B.V. Publicador: Elsevier B.V.
Tipo: Artigo de Revista Científica Formato: 1752-1757
Português
Relevância na Pesquisa
55.86%
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP); Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq); Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES); Processo FAPESP: 10/17877-4; Processo FAPESP: 10/19136-1; Processo FAPESP: 11/09047-4; Introduction: This clinical study has investigated the antigenic activity of bacterial contents from exudates of acute apical abscesses (AAAs) and their paired root canal contents regarding the stimulation capacity by levels of interleukin (IL)-1 beta and tumor necrosis factor alpha (TNF-alpha) throughout the root canal treatment against macrophage cells. Methods: Paired samples of infected root canals and exudates of AAAs were collected from 10 subjects. Endodontic contents were sampled before (root canal sample [RCS] 1) and after chemomechanical preparation (RCS2) and after 30 days of intracanal medication with calcium hydroxide + chlorhexidine gel (Ca[OH](2) + CHX gel) (RCS3). Polymerase chain reaction (16S rDNA) was used for detection of the target bacteria, whereas limulus amebocyte lysate was used to measure endotoxin levels. Raw 264.7 macrophages were stimulated with AAA exudates from endodontic contents sampled in different moments of root canal treatment. Enzyme-linked immunosorbent assays were used to measure the levels of TNF-alpha and 11-1 beta. Results: Parvimonas micra...

Investigação de marcadores de epileptogênese no modelo animal zebrafish; Markers of epileptogenesis in the zebrafish seizure model

Patricia Gonçalves Barbalho
Fonte: Biblioteca Digital da Unicamp Publicador: Biblioteca Digital da Unicamp
Tipo: Dissertação de Mestrado Formato: application/pdf
Publicado em 29/07/2013 Português
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55.87%
O Danio rerio é um peixe teleósteo popularmente conhecido como zebrafish que têm se destacado como modelo animal favorável para investigações genéticas devido à facilidade de manipulação in vivo, por sua transparência nas fases embrionária e larval e por seu desenvolvimento externo. Recentemente, foi demonstrado que o zebrafish é capaz de exibir padrão comportamental e alteração da atividade eletrográfica durante crise epiléptica como visto em roedores, tornando-o um modelo promissor para as investigações moleculares das epilepsias. Os estudos sobre os diferentes eventos já conhecidos das epilepsias no zebrafish estão apenas começando e, portanto, há ainda muito que ser investigado para uma melhor caracterização deste modelo para estudos em epilepsia. Estudos clínicos e em modelos animais mostraram que a crise epiléptica eleva os níveis da interleucina-1 beta e induz morte neuronal. Nesse sentido, o presente trabalho se propôs a investigar (i) o perfil temporal de expressão do transcrito do gene da interleucina-1 beta (il1b) no cérebro imaturo e adulto do zebrafish após a indução de crise epiléptica pelo agente químico Pentilenotetrazol por transcriptase reversa-PCR quantitativa e também, sua relação da expressão com a idade em que é realizada a indução da crise no cérebro imaturo e (ii) a morte neuronal pela histoquímica do Fluoro-Jade B (FJB) no cérebro imaturo e adulto do zebrafish após a indução de crise epiléptica pelo agente químico Pentilenotetrazol. Neste trabalho conseguimos estabelecer com sucesso as condições ideais para o acasalamento desta espécie e obtenção de embriões e...

Cross-talk between cyclooxygenase and nitric oxide pathways: prostaglandin E2 negatively modulates induction of nitric oxide synthase by interleukin 1.

Tetsuka, T; Daphna-Iken, D; Srivastava, S K; Baier, L D; DuMaine, J; Morrison, A R
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em 06/12/1994 Português
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55.86%
The inflammatory cytokine interleukin 1 beta (IL-1 beta) induces both cyclooxygenase (COX) and nitric oxide synthase (NOS) with increases in the release of prostaglandin (PG) and nitric oxide (NO) by mesangial cells. Recently, activation of the COX enzyme by NO has been described. However, the effects of COX products (PGs) on the NO pathway have not been fully clarified. Thus we determined the effect of COX inhibition and exogenous PGs on NO production and NOS induction in rat mesangial cells. A COX inhibitor, indomethacin, enhanced IL-1 beta-induced steady-state level of the inducible NOS (iNOS) mRNA and nitrite production. The effect of indomethacin was dose dependently reversed by the replacement of endogenous PGE2 with exogenous PGE2, which is the predominant product of the COX pathway in rat mesangial cells. In contrast to PGE2, a stable analog of PGI2, carba prostacyclin, enhanced IL-1 beta-induced iNOS mRNA levels and nitrite production. Forskolin, an activator of the adenylate cyclase, mimicked the effect of carba prostacyclin but not PGE2. These data suggest that (i) endogenous PGE2 downregulates iNOS induction, (ii) this inhibitory effect of PGE2 on iNOS induction is not mediated by activation of adenylate cyclase, and (iii) exogenous PGI2 stimulates COX induction possibly by activation of adenylate cyclase.

Enhanced immunogenicity of a sequence derived from hepatitis B virus surface antigen in a composite peptide that includes the immunostimulatory region from human interleukin 1.

Rao, K V; Nayak, A R
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /07/1990 Português
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The effect on immunogenicity of coupling the immunostimulatory nonapeptide sequence (residues 163-171) from human interleukin 1 beta (IL-1 beta) to a small immunogen was examined. A 21-amino acid sequence spanning positions 12-32 on the large protein of hepatitis B surface antigen was chosen as a model. Three peptides were synthesized corresponding to the IL-1 beta-derived sequence [peptide IL-(163-171)], the hepatitis B surface antigen-derived sequence [peptide S1-(12-32)] and a composite peptide that included both these sequences separated by a spacer of two glycine residues [peptide S1-(12-32)-IL-(163-171)]. In an in vitro thymocyte proliferation assay, both peptides S1-(12-32)-IL-(163-171) and IL-(163-171) showed comparable activity, whereas peptide S1-(12-32) was inactive. Groups of five to seven mice each from C3H/CH, BALB/c, SJL/J, and C57BL/6 strains were immunized with equimolar amounts of either peptide S1-(12-32), peptide S1-(12-32)-IL-(163-171), or a mixture of peptides S1-(12-32) and IL-(163-171), and sera were screened for anti-S1-(12-32) antibodies. In all strains, peptide S1-(12-32)-IL-(163-171) elicited an increased primary and secondary anti-S1-(12-32) antibody response compared to the other two groups. Further, peptide S1-(12-32)-IL-(163-171) also induced an increased number of responders to primary immunization...

Monocyte responses to sulfatide from Mycobacterium tuberculosis: inhibition of priming for enhanced release of superoxide, associated with increased secretion of interleukin-1 and tumor necrosis factor alpha, and altered protein phosphorylation.

Brozna, J P; Horan, M; Rademacher, J M; Pabst, K M; Pabst, M J
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /08/1991 Português
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In monocytes, sulfatide, a lipid from Mycobacterium tuberculosis, blocked priming for enhanced release of superoxide (O2-) by the macrophage activating factors lipopolysaccharide, gamma interferon, interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), and muramyl dipeptide. Sulfatide, in the presence of lipopolysaccharide, also caused increased secretion of IL-1 beta and TNF-alpha into monocyte culture medium. Sulfatide altered the pattern of phosphorylation of monocyte proteins. Cell lysates prepared from monocytes treated with sulfatide showed decreased activity of protein kinase C, but sulfatide did not directly inhibit protein kinase C activity when added to lysates. A known inhibitor of protein kinase C, staurosporine, also inhibited O2- release and caused increased secretion of IL-1 beta. Thus, sulfatide appeared to indirectly affect protein kinase C, implicating protein kinase C as part of the mechanism of priming. Because sulfatide blocked priming for enhanced release of O2-, which could interfere with monocyte bactericidal activity, while causing enhanced secretion of IL-1 beta and TNF-alpha, which could promote formation of granulomata, sulfatide might be an important factor in the pathogenesis of M. tuberculosis.

Activation of human monocytes by Streptococcus mutans serotype f polysaccharide: immunoglobulin G Fc receptor expression and tumor necrosis factor and interleukin-1 production.

Benabdelmoumene, S; Dumont, S; Petit, C; Poindron, P; Wachsmann, D; Klein, J P
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /09/1991 Português
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Streptococcus mutans serotype f polysaccharide (poly f) was prepared from S. mutans whole cells by autoclaving. The poly f was purified by chromatography on DEAE Trisacryl M and Bio-Gel P100, treated with insoluble pronase, and resubjected to chromatography on DEAE Trisacryl M. Normal human blood monocytes, stimulated in vitro with purified poly f, produced extracellular tumor necrosis factor alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) in a dose-dependent fashion as determined by a heterologous two-site sandwich enzyme-linked immunosorbent assay. Poly f also increased the expression of monocyte cell surface receptors for the Fc part of human immunoglobulin G, activity which is correlated with an increase of the phagocytic activity of the stimulated monocytes. Polymyxin B had no effect on TNF-alpha and IL-1 beta release. Neutralization assays with anti-recombinant human TNF-alpha and anti-recombinant human IL-1 beta immunoglobulin G confirmed the fact that the cytotoxic and mitogenic mediators released by the poly f-stimulated monocytes were mainly TNF-alpha and IL-1 beta.

Interleukin 1 beta induces the formation of nitric oxide by beta-cells purified from rodent islets of Langerhans. Evidence for the beta-cell as a source and site of action of nitric oxide.

Corbett, J A; Wang, J L; Sweetland, M A; Lancaster, J R; McDaniel, M L
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /12/1992 Português
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Nitric oxide has recently been implicated as the effector molecule that mediates IL-1 beta-induced inhibition of glucose-stimulated insulin secretion and beta-cell specific destruction. The pancreatic islet represents a heterogeneous cell population containing both endocrine cells (beta-[insulin], alpha-]glucagon], gamma[somatostatin], and PP-[polypeptide] secreting cells) and non-endocrine cells (fibroblast, macrophage, endothelial, and dendritic cells). The purpose of this investigation was to determine if the beta-cell, which is selectively destroyed during insulin-dependent diabetes mellitus, is both a source of IL-1 beta-induced nitric oxide production and also a site of action of this free radical. Pretreatment of beta-cells, purified by FACS with IL-1 beta results in a 40% inhibition of glucose-stimulated insulin secretion that is prevented by the nitric oxide synthase inhibitor, NG-monomethyl-L-arginine (NMMA). IL-1 beta induces the formation of nitric oxide by purified beta-cells as evidenced by the accumulation of cGMP, which is blocked by NMMA. IL-1 beta also induces the accumulation of cGMP by the insulinoma cell line Rin-m5F, and both NMMA as well as the protein synthesis inhibitor cycloheximide prevent this cGMP accumulation. Iron-sulfur proteins appear to be intracellular targets of nitric oxide. IL-1 beta induces the formation of an iron-dinitrosyl complex by Rin-m5F cells indicating that nitric oxide mediates the destruction of iron-sulfur clusters of iron containing enzymes. This is further demonstrated by IL-1 beta-induced inhibition of glucose oxidation by purified beta-cells...

Value of synovial fluid interleukin-1 beta determination in predicting the outcome of psoriatic monoarthritis.

Punzi, L; Bertazzolo, N; Pianon, M; Rizzi, E; Rossini, P; Gambari, P
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /09/1996 Português
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55.88%
OBJECTIVE: To investigate the value of synovial fluid analysis in predicting the outcome of psoriatic monoarthritis. METHODS: In synovial fluid from knee joints of 18 patients with psoriatic monoarthritis lasting less than six months, white blood cell count, acid phosphatase, lysozyme, and interleukin (IL)-1 beta were determined. ESR and serum C reactive protein were also measured. To define the outcome, the patients were monitored for at least three years and then subdivided into those with polyarthritis and those without. RESULTS: Among the blood and synovial fluid indices considered, synovial fluid IL-1 beta was the only variable which differed between the patients who developed polyarthritis, within three years and those without polyarthritis after this time, at 20.82(SD 8.79) v 4.19(4.73) pg ml-1, P < 0.0001). A correlation was found between synovial fluid IL-1 beta concentrations and the number of affected joints after three years (r = 0.739, P < 0.0001). CONCLUSIONS: Determination of synovial fluid IL-1 beta at disease onset may be useful in revealing the outcome of psoriatic monoarthritis since, among the variables considered in our study, this was the only one capable of predicting the evolution of monoarticular psoriatic arthritis to polyarthritis.

Interleukin-1 beta regulation of fibroblast proteoglycan synthesis involves a decrease in versican steady-state mRNA levels.

Qwarnström, E E; Järveläinen, H T; Kinsella, M G; Ostberg, C O; Sandell, L J; Page, R C; Wight, T N
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em 01/09/1993 Português
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55.87%
This study investigates the effects of interleukin (IL)-1 beta on proteoglycan metabolism by fibroblasts surrounded by endogenous extracellular matrix. In both three-dimensional matrix cultures and long-term monolayer cultures IL-1 beta caused a significant decrease in synthesis and deposition of sulphated proteoglycans, but had no effect on release of deposited material. The decrease in synthesis became successively more pronounced, and corresponded to 40-60% of the control after 72 h incubation. The reduction was almost totally accounted for by an effect on the chondroitin ABC-lyase-sensitive proteoglycans. Gel electrophoresis showed a significant decrease in a high-molecular-mass chondroitin ABC-lyase-sensitive proteoglycan after incubation with IL-1 beta. Northern-blot analyses of total RNA revealed a pronounced decrease in the steady-state mRNA levels of versican, the large chondroitin sulphate, with levels corresponding to 10-30% of controls. In comparison, the steady-state mRNA level for decorin, the major sulphated proteoglycan synthesized by the cells, was only slightly affected. The prominent decrease in synthesis of sulphated proteoglycans induced in long-term fibroblast cultures, including the pronounced decrease in versican steady-state mRNA levels...

ACTH response induced in capsaicin-desensitized rats by intravenous injection of interleukin-1 or prostaglandin E.

Watanabe, T; Morimoto, A; Tan, N; Makisumi, T; Shimada, S G; Nakamori, T; Murakami, N
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em 15/02/1994 Português
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1. We investigated whether afferent nerves are involved in the development of adrenocorticotrophic hormone (ACTH) responses induced either by systemic administration of interleukin-1 beta (IL-1 beta) and prostaglandin E2, or by psychological stress. The capsaicin desensitization method was used to impair afferent C fibres and we compared the ACTH responses between capsaicin desensitized and vehicle pretreated control rats. 2. The present results showed that the capsaicin desensitized rats had significantly smaller increases in plasma ACTH than the control rats in response to intravenous injection of IL-1 beta or prostaglandin E2. 3. There were no significant differences between the capsaicin desensitized and control rats in the ACTH responses induced by cage switch stress. 4. The capsaicin desensitized rats responded to intravenous injection of corticotrophin releasing factor (CRF) with a greater increase in the plasma level of ACTH than the control rats, indicating that capsaicin pretreatment resulted in augmentation of pituitary gland sensitivity to CRF. 5. These results suggest that afferent neurons play an important role in the ACTH responses induced by systemic injection of IL-1 beta or prostaglandin E2.

Down-regulation of cyclooxygenase-2 (COX-2) by interleukin-1 receptor antagonist in human monocytes.

Porreca, E; Reale, M; Di Febbo, C; Di Gioacchino, M; Barbacane, R C; Castellani, M L; Baccante, G; Conti, P; Cuccurullo, F
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /11/1996 Português
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Cyclooxygenase (COX) is the key rate-limiting enzyme in the synthesis of prostanoids from arachidonic acid. Two isoforms of COX have been described in mammalian cells, referred to as cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). COX-1 is a constitutively expressed enzyme; COX-2 is an inducible enzyme that appears to be expressed in inflamed tissue and following exposure to growth factors or cytokines, such as interleukin-1 (IL-1). The aim of the present study was to test if the antagonism on the binding of IL-1 to its cell-surface receptor by human recombinant IL-1 receptor antagonist (hrIL-1ra) may control the COX mRNA expression and prostaglandin E2 (PGE2) production by human monocyte cultures. Northern blot studies showed that hrIL-ra (500 ng/ml) had a strong inhibitory effect on inducible COX activity. The effect was evident after 6 hr incubation (2.7-fold decrease of mRNA COX-2 transcripts); and about a threefold decrease at 24hr incubation. A non-significant effect was observed with COX-1 transcripts. Induced PGE2 production by monocyte cultures treated with lipopolysaccharide (LPS) or interleukin-1 beta (IL-1 beta) was strongly inhibited in the presence of hrIL-1ra (500 ng/ml). In addition, a significant inhibition of COX-2 protein expression...

Human interleukin 1 beta is not secreted from hamster fibroblasts when expressed constitutively from a transfected cDNA

Fonte: The Rockefeller University Press Publicador: The Rockefeller University Press
Tipo: Artigo de Revista Científica
Publicado em 01/08/1988 Português
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To understand the secretion and processing of interleukin-1 (IL-1), a Chinese hamster fibroblast cell line (R1610) was transfected with a human IL-1 beta cDNA under the control of the SV40 early promoter and linked to the gene for neomycin resistance. After selecting for transfected cells resistant to G418, two clones were found to constitutively express the IL-1 beta 31-kD precursor which was almost exclusively located in the cytosol. Pulse-chase experiments failed to show any secretion of IL-1 and very little IL-1 activity was detectable in cell supernatants. Furthermore, surface membrane IL-1 activity could not be detected, although low levels of activity could be released upon brief trypsin treatment. Therefore, unlike monocytes, these fibroblast cells lack the mechanism for secreting and processing of IL-1 beta.

Combined interleukin 1/interleukin 2 therapy of mice injected with highly metastatic Friend leukemia cells: host antitumor mechanisms and marked effects on established metastases

Fonte: The Rockefeller University Press Publicador: The Rockefeller University Press
Tipo: Artigo de Revista Científica
Publicado em 01/02/1991 Português
Relevância na Pesquisa
55.86%
Peritumoral injection of recombinant human interleukin 1 beta (IL-1 beta) in mice transplanted subcutaneously with Friend erythroleukemia cells (FLC) resulted in a marked increase in survival time and inhibition of metastatic tumor growth in liver and spleen. In contract, IL-2 treatment alone did not significantly inhibit the development of FLC metastases. A synergistic antitumor effect was observed after combined IL-1/IL-2 therapy of these mice. The antitumor action of IL- 1/IL-2 treatment was abolished or markedly reduced in mice treated with antibodies to CD4 or CD8 antigens, whereas antibodies to asialo-GM1 were ineffective. A clear-cut increase in the percentage of CD4+ cells was observed in the spleens of cytokine-treated mice on days 17 and 23. On day 23 of cytokine therapy, CD8+ cells were increased in both spleens and lymph nodes. On day 17, infiltrates of host-reactive cells (i.e., lymphocytes, granulocytes, and monocytes) were observed in both spleen and liver from FLC-injected mice treated with IL-1/IL-2, in association with tumor cells. On days 17 and 23, spleen cells and cells recovered from mesenteric lymph nodes of IL-1/IL-2-treated mice exerted a potent antitumor effect as determined by Winn assay experiments. This antitumor activity was abolished by preincubation of spleen cells with anti-CD8 antibody...

Peripheral endotoxin induces hypothalamic immunoreactive interleukin-1 beta in the rat.

Hillhouse, E. W.; Mosley, K.
Fonte: Nature Publishing Group Publicador: Nature Publishing Group
Tipo: Artigo de Revista Científica
Publicado em /06/1993 Português
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55.88%
Interleukin-1 (IL-1) is a polypeptide produced by a variety of cells and contributes to the general host response to inflammation. It displays a wide spectrum of inflammatory, metabolic, physiological, haematopoietic and immunological activities. Brain cells, including neurones, microglia, endothelial cells and astrocytes can all produce IL-1 beta in response to various physiological and pathological stimuli. In this report we show that peripherally administered endotoxin stimulates the appearance of immunoreactive IL-1 beta (IL-1 beta) in the rat hypothalamus as measured by an ultrasensitive, highly specific enzyme amplified immunometric assay for rat IL-1 beta.

Dual control of C-reactive protein gene expression by interleukin-1 and interleukin-6.

Ganter, U; Arcone, R; Toniatti, C; Morrone, G; Ciliberto, G
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em 01/12/1989 Português
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Human C-reactive protein (CRP) is the major acute phase reactant during acute inflammation. The human CRP promoter is expressed in an inducible and cell-specific manner when linked to the bacterial CAT gene and transfected into human hepatoma cell cultures. In this paper we analyze the effect of several recombinant cytokines or CRP promoter inducibility in human Hep3B cells. When cytokines are tested singly the major inducer of CRP-CAT fusions is interleukin-6 (IL-6). Maximal CAT gene expression, however, is only achieved when both interleukin-1 beta (IL-1 beta) and IL-6 are present. The response to the two cytokines is cooperative. Cooperativity is maintained when the CRP promoter is linked to a different coding region, that of the bacterial neomycin phosphotransferase II gene. With a series of 5' and 3' deletions we show the existence of two distinct and independent regions responsive to IL-6 and located upstream to the TATA box. The IL-1 effect is exerted at the level of downstream sequences that are probably important for optimal mRNA translatability or nuclear-cytoplasmic transport. Inducibility is not influenced by the activation of protein kinases C or A and does not require new protein synthesis.

Dexamethasone differentially affects interleukin 1 beta- and cyclic AMP-induced nitric oxide synthase mRNA expression in renal mesangial cells.

Kunz, D; Walker, G; Pfeilschifter, J
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em 01/12/1994 Português
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Inducible nitric oxide synthase (iNOS) is expressed in renal mesangial cells in response to two principal classes of activating signals that interact in a synergistic fashion. These two groups of activators comprise inflammatory cytokines such as interleukin (IL)-1 beta or tumour necrosis factor alpha and agents that elevate cellular levels of cyclic AMP (cAMP). We examined whether dexamethasone differentially affects iNOS induction in response to IL-1 beta and a membrane-permeable cAMP analogue, N6,O-2'-dibutyryladenosine 3',5'-phosphate (Bt2cAMP). Nanomolar concentrations of dexamethasone suppress IL-1 beta- as well as Bt2cAMP-induced iNOS protein expression and production of nitrite, the stable end product of nitric oxide (NO) formation. In contrast, dexamethasone prevents induction of iNOS mRNA in response to Bt2cAMP without affecting IL-1 beta-triggered increase in iNOS mRNA levels. These data suggest that dexamethasone acts at different levels, depending on the stimulus used to suppress iNOS induction in mesangial cells.