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Caspase-1 is involved in the genesis of inflammatory hypernociception by contributing to peripheral IL-1 beta maturation

CUNHA, Thiago M.; TALBOT, Jhimmy; PINTO, Larissa G.; VIEIRA, Silvio M.; SOUZA, Guilherme R.; GUERRERO, Ana T.; SONEGO, Fabiane; VERRI JR., Waldiceu A.; ZAMBONI, Dario S.; FERREIRA, Sergio H.; CUNHA, Fernando Q.
Fonte: BIOMED CENTRAL LTD Publicador: BIOMED CENTRAL LTD
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
75.92%
Background: Caspase-1 is a cysteine protease responsible for the processing and secretion of IL-1 beta and IL-18, which are closely related to the induction of inflammation. However, limited evidence addresses the participation of caspase-1 in inflammatory pain. Here, we investigated the role of caspase-1 in inflammatory hypernociception (a decrease in the nociceptive threshold) using caspase-1 deficient mice (casp1-/-). Results: Mechanical inflammatory hypernociception was evaluated using an electronic version of the von Frey test. The production of cytokines, PGE(2) and neutrophil migration were evaluated by ELISA, radioimmunoassay and myeloperoxidase activity, respectively. The interleukin (IL)-1 beta and cyclooxygenase (COX)-2 protein expression were evaluated by western blotting. The mechanical hypernociception induced by intraplantar injection of carrageenin, tumour necrosis factor (TNF)alpha and CXCL1/KC was reduced in casp1-/- mice compared with WT mice. However, the hypernociception induced by IL-1 beta and PGE(2) did not differ in WT and casp1-/- mice. Carrageenin-induced TNF-alpha and CXCL1/KC production and neutrophil recruitment in the paws of WT mice were not different from casp1-/- mice, while the maturation of IL-1 beta was reduced in casp1-/- mice. Furthermore...

Central substance P NK(1) receptors are involved in fever induced by LPS but not by IL-1 beta and CCL3/MIP-1 alpha in rats

REIS, R. C.; BRITO, H. O.; FRAGA, D.; CABRINI, D. A.; ZAMPRONIO, A. R.
Fonte: ELSEVIER SCIENCE BV Publicador: ELSEVIER SCIENCE BV
Tipo: Artigo de Revista Científica
Português
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75.9%
Substance P (SP) is a neuropeptide that can modulate inflammatory mediator release through activation of NK(1) receptors (NK(1)R). Some studies have also suggested the involvement of SP in lipopolysaccharide (LPS)-induced fever. However, the precise contribution of this neuropeptide to the pathways activated during fever is unknown. In this study we investigated the effect of a selective NK(1)R antagonist, SR140333B, on the febrile response induced by LPS and cytokines. Our results show that the systemic injection of SR140333B did not modify the fever induced by LPS at a dose that is able to reduce protein extravasation induced by SP in the skin. On the other hand, intracerebroventricular administration of 5R140333B significantly reduced the fever induced by peripheral injection of LPS. These data emphasize an important role for SP in the central nervous system during the febrile response to LPS, and are reinforced by the fact that intracerebroventricular injection of SP also induced fever in a dose-dependent manner in captopril-treated rats. Considering that the febrile response can result from the generation of several endogenous pyrogens, among them interleukin (IL)-1 beta and macrophage inflammatory protein-1 alpha (CCL3/MIP-1 alpha)...

Interleukin-1 beta Serum Levels is Increased in Antidepressant-Free Elderly Depressed Patients

DINIZ, Breno Satler; TEIXEIRA, Antonio Lucio; TALIB, Leda; GATTAZ, Wagner Farid; FORLENZA, Orestes Vicente
Fonte: LIPPINCOTT WILLIAMS & WILKINS Publicador: LIPPINCOTT WILLIAMS & WILKINS
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
95.97%
Objective: To assess the serum levels of interleukin 1 beta (IL-1 beta) in elderly depressed patients in comparison with nondepressed healthy elderly subjects. Design: Cross-sectional study. Setting: Tertiary memory clinic. Participants: Twenty-three antidepressant-free elderly depressed patients and 44 nondepressed healthy elderly comparison group were enrolled to this study. Measurement: Serum IL-1 beta levels were determined with highly sensitive colorimetric sandwich enzyme-linked immunosorbent assay. Severity of the depressive episode was determined by scores on the Hamilton Depression Scale-21 item and cognitive performance by the scores on the Cambridge Cognition Examination, Mini Mental State Examination clock drawing test, and verbal fluency. Results: IL-1 beta serum levels were increased in elderly patients versus nondepressed elderly (t = 2.21, df = 65, p = 0.04). After categorizing elderly depressed subjects into late onset (LOD) versus early onset (EOD), patients with EOD had the highest IL-1 beta levels, when compared with nondepressed elderly patients and patients with LOD in analysis of variance (F = 4.9, df = 2, 64, p < 0.01). Conclusions: Late-life depression is associated with higher IL-1 beta levels suggesting that increased proinflammatory state may play a role in the physiopathology of depression in the elderly. The authors further show that this might be more prominent in those patients with EOD geriatric depression. (Am J Geriatr Psychiatry 2010; 18: 172-176); Rede Instituto Brasileiro de Neurociencia; FAPESP Fundacao de Amparo a Pesquisa do Estado de Sao Paulo[02/12633-7]; Associacao Beneficente Alzira Denise Hertzog da Silva (ABADHS); CAPES...

Stromal interleukin-1 expression in the cornea after haze-associated injury

BARBOSA, F. L.; CHAURASIA, S. S.; KAUR, H.; MEDEIROS, F. W. de; AGRAWAL, V.; WILSON, S. 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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66.02%
The purpose of this study was to determine whether myofibroblasts or other cells in the stroma in the cornea produce interleukin (IL)-1 alpha or IL-1 beta that could modulate myofibroblast viability in corneas with haze after photorefractive keratectomy (PRK). Twenty-four female rabbits had haze-generating PRK for 9 diopters of myopia and were sacrificed at 1 week, 2 weeks, 3 weeks or 4 weeks after surgery. Corneal rims were removed, frozen in OCT at -80 degrees C, and analyzed by immunocytochemistry using primary antibodies to IL-1 alpha, IL-1 beta and alpha smooth muscle actin (SMA). Double immunostaining was performed for the co-localization of SMA with IL-1 alpha or IL-1 beta. Central dense haze and peripheral slight haze regions of each cornea were analyzed. SMA+ cells that expressed IL-1 alpha protein were detected in both regions of the corneas at most time points following PRK. However, in the haze region at the 1,3 and 4 week time points, significantly more (p < 0.01) SMA cells did not express IL-1 alpha. Also, in the haze region at all three time points, significantly more (p < 0.01) SMA- cells than SMA+ cells expressed interleukin-1 alpha protein. IL-1 beta expression patterns in SMA+ and SMA- stromal cells was similar to that of IL-1 alpha after PRK. Previous studies have demonstrated that IL-1 alpha or IL-1 beta triggers myofibroblast apoptosis in vitro...

Increased Serum IL-1 beta Level in Alzheimer`s Disease and Mild Cognitive Impairment

FORLENZA, Orestes Vicente; DINIZ, Breno Satler; TALIB, Leda Leme; MENDONCA, Vanessa Amaral; OJOPI, Elida B.; GATTAZ, Wagner Farid; TEIXEIRA, Antonio Lucio
Fonte: KARGER Publicador: KARGER
Tipo: Artigo de Revista Científica
Português
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85.93%
Background/Aims: Abnormal inflammatory response has been associated to the pathogenesis of Alzheimer`s disease (AD) and may be a marker of an ongoing neurodegenerative process. The aim of this study was to evaluate the serum levels of interleukin-1 beta (IL-1 beta) in patients with mild cognitive impairment (MCI) and AD. Methods: One hundred and sixty-three older adults ( 58 with mild to moderate AD, 74 with MCI and 31 healthy controls) were recruited for this study. Serum IL-1 beta levels were measured by ELISA. Patients with MCI were subcategorized in single-domain amnestic (aMCI), nonamnestic (naMCI), and multiple-domain (mdMCI) subtypes. Results: Patients with AD and MCI ( all subtypes) had a significant increase in serum IL-1 beta levels as compared to controls (p = 0.03). Patients with mdMCI had serum IL-1 beta levels comparable to those with AD, and significantly higher than those observed in aMCI and naMCI ( p = 0.02). Discussion: The present study provides evidence that inflammatory mechanisms, represented by elevated IL-1 beta, are observed in patients with MCI, specifically in those with impairment in multiple cognitive domains. As these patients are at higher risk of conversion to dementia, we propose that an increased serum IL-1 beta level is a stage marker of the ongoing brain neurodegeneration in the continuum between normal ageing and AD. Copyright (C) 2009 S. Karger AG...

P2X(7) receptor activation amplifies lipopolysaccharide-induced vascular hyporeactivity via interleukin-1 beta release

CHIAO, Chin-Wei; TOSTES, Rita C.; WEBB, R. Clinton
Fonte: AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS Publicador: AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
Tipo: Artigo de Revista Científica
Português
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75.94%
Lipopolysaccharide (LPS) stimulates cytoplasmic accumulation of pro-interleukin (IL)-1 beta. Activation of P2X(7) receptors stimulates conversion of pro-IL-1 beta into mature IL-1 beta, which is then secreted. Because both LPS (in vivo) and IL-1 beta (in vitro) decrease vascular reactivity to contractile agents, we hypothesized the following: 1) P2X(7) receptor activation contributes to LPS-induced vascular hyporeactivity, and 2) IL-1 beta mediates this change. Thoracic aortas were obtained from 12-week-old male C57BL/6 mice. The aortic rings were incubated for 24 h in Dulbecco`s modified Eagle`s medium, LPS, benzoylbenzoyl-ATP (BzATP; P2X(7) receptor agonist), LPS plus BzATP, oxidized ATP (oATP; P2X(7) receptor antagonist), or oATP plus LPS plus BzATP. After the treatment, the rings were either mounted in a myograph for evaluation of contractile activity or homogenized for IL-1 beta and inducible nitric-oxide synthase (iNOS) protein measurement. In endothelium-intact aortic rings, phenylephrine (PE)-induced contractions were not altered by incubation with LPS or BzATP, but they significantly decreased in aortic rings incubated with LPS plus BzATP. Treatment with oATP or IL-1ra (IL-1 beta receptor antagonist) reversed LPS plus BzATP-induced hyporeactivity to PE. In the presence of N(G)-nitro-L-arginine methyl ester or N-([3-(aminomethyl) phenyl] methyl) ethanimidamide (selective iNOS inhibitor)...

Low level laser therapy (LLLT) decreases pulmonary microvascular leakage, neutrophil influx and IL-1 beta levels in airway and lung from rat subjected to LPS-induced inflammation

AIMBIRE, F.; OLIVEIRA, A. P. Ligeiro de; ALBERTINI, R.; CORREA, J. C.; CAMPOS, C. B. Ladeira de; LYON, J. P.; SILVA JR., J. A.; COSTA, M. S.
Fonte: SPRINGER/PLENUM PUBLISHERS Publicador: SPRINGER/PLENUM PUBLISHERS
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
75.9%
Background and Objective. Low level laser therapy (LLLT) is a known anti-inflammatory therapy. Herein we studied the effect of LLLT on lung permeability and the IL-1 beta level in LPS-induced pulmonary inflammation. Study Design/Methodology. Rats were divided into 12 groups (n = 7 for each group). Lung permeability was measured by quantifying extravasated albumin concentration in lung homogenate, inflammatory cells influx was determined by myeloperoxidase activity, IL-1P in BAL was determined by ELISA and IL-1P mRNA expression in trachea was evaluated by RT-PCR. The rats were irradiated on the skin over the upper bronchus at the site of tracheotomy after LPS. Results. LLLT attenuated lung permeability. In addition, there was reduced neutrophil influx, myeloperoxidase activity and both IL-1 beta in BAL and IL-1 beta mRNA expression in trachea obtained from animals subjected to LPS-induced inflammation. Conclusion. LLLT reduced the lung permeability by a mechanism in which the IL-1 beta seems to have an important role.

Evidence of a relationship between aversive learning and hippocampal interleukin 1 beta levels in neonatal handled rats

Nunes, Wagner de Paula
Fonte: Universidade Federal do Rio Grande do Sul Publicador: Universidade Federal do Rio Grande do Sul
Tipo: Trabalho de Conclusão de Curso Formato: application/pdf
Português
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96.02%
The Neonatal Handling (NH) model presents a “blunted” corticosterone response to stress as well as an enhancement in contextual fear tasks. So the aim of this work was to examine a possible relationship between diminished imunosuppression over Interleukin 1 beta (IL-1) hippocampal levels and enhancement in aversive learning. To achieve that, we subjected male handled Wistar rats 30-35 and 90 days old to an inhibitory avoidance task, comparing the avoidance scores with respective hippocampal IL-1 levels at different time points. We found that handled adult animals learned the aversive task concomitantly with higher levels of hippocampal interleukin 1 beta 2h after footshock, while control animals showed diminished aversive learning and lower IL-1 beta levels at the same time. In the other hand, both handled and non-handled juvenile rats learned the aversive task, with no signal of immunosuppressant efect over interleukin 1 beta. However, basal levels of IL-1 beta were different between handled and non-handled animals in both ages, pointing a novel neuroimmunomodulation involvement to the NH model.

Low protein diet confers resistance to the inhibitory effects of interleukin1 beta on insulin secretion in pancreatic islets

Vieira, E. C.; Carneiro, E. M.; Latorraca, M. Q.; Delguingaro-Augusto, V; Amaral, MEC; Bosqueiro, JR; Boschero, A. C.
Fonte: Elsevier B.V. Publicador: Elsevier B.V.
Tipo: Artigo de Revista Científica Formato: 285-291
Português
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75.93%
High protein content in the diet during childhood and adolescence has been associated to the onset insulin-dependent diabetes mellitus. We investigated the effect of interleukin-1 beta (IL-I beta) on insulin secretion, glucose metabolism, and nitrite formation by islets isolated from rats fed with normal protein (NP, 17%) or low protein (LP, 6%) after weaning. Pretreatment of islets with IL-1 beta for 1 h or 34 h inhibited the insulin secretion induced by glucose in both groups, but it was less marked in LP than in NP group. Islets from LP rats exhibited a decreased IL-1 beta -induced nitric oxide (NO) production, lower inhibition of D-[(UC)-C-14]-glucose oxidation to (CO2)-C-14, and less pronounced effect of IL-1 beta on alpha -ketoisocaproic acid-induced insulin secretion than NP islets. However, when the islets were stimulated by high concentrations of K+ the inhibitory effect of IL-1 beta on insulin secretion was not different between groups. In conclusion, protein restriction protects beta -cells of the deleterious effect of IL-1 beta, apparently, by decreasing NO production. The lower NO generation in islets from protein deprived rats may be due to increased free fatty acids oxidation and consequent alteration in Ca2+ homeostasis. (C) 2001 Elsevier B.V. All rights reserved.

Differential usage of NF-kappa B activating signals by IL-1 beta and TNF-alpha in pancreatic beta cells

Ortis, F.; Miani, M.; Colli, M. L.; Cunha, D. A.; Gurzov, E. N.; Allagnat, F.; Chariot, A.; Eizirik, D. L.
Fonte: Elsevier; Amsterdam Publicador: Elsevier; Amsterdam
Tipo: Artigo de Revista Científica
Português
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75.94%
The cytokines interleukin (IL)-1 beta and tumor necrosis factor (TNF)-alpha induce beta-cell death in type 1 diabetes via NF-kappa B activation. IL-1 beta induces a more marked NF-kappa B activation than TNF-alpha, with higher expression of genes involved in beta-cell dysfunction and death. We show here a differential usage of the IKK complex by IL-1 beta and TNF-alpha in beta-cells. While TNF-alpha uses IKK complexes containing both IKK alpha and IKK beta, IL-1 beta induces complexes with IKKa only; this effect is achieved by induction of IKK beta degradation via the proteasome. Both IKK gamma and activation of the TRAF6-TAK1-JNK pathway are involved in IL-1 beta-induced IKK beta degradation. (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.; Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP); Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Effects of erythromycin on γ-glutamyl cysteine synthetase and interleukin-1β in hyperoxia-exposed lung tissue of premature newborn rats

Cai,Cheng; Qiu,Gang; Gong,Xiaohui; Chen,Yihuan; Zhao,Huanhu
Fonte: Sociedade Brasileira de Pediatria Publicador: Sociedade Brasileira de Pediatria
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/10/2014 Português
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75.9%
Objetivo: Explorar o efeito da eritromicina sobre lesões pulmonares induzidas por hiperóxia. Métodos: Uma prole de ratos Sprague-Dawley (SD) prematuros com um dia de vida foi dividida aleatoriamente em quatro grupos: grupo 1 ar + cloreto de sódio, grupo 2 ar + eritromicina, grupo 3 hiperóxia + cloreto de sódio e grupo 4 hiperóxia + eritromicina. Com um, sete e 14 dias de exposição, foram detectadas Glutationa (GSH) e Interleucina-1 beta (IL-1 beta) pelo ensaio imunossorvente ligado à enzima (ELISA), e o ácido bicinconinico (BCA) foi utilizado para detectar a proteína GSH. O mRNA da γ-glutamil-cisteina-sintetase (γ-GCS) foi detectado por reação em cadeia da polimerase via transcriptase reversa (RT-PCR). Resultados: Comparadas ao grupo 1, as expressões do mRNA da GSH e da γ-GCS no grupo 3 aumentaram significativamente com um e sete dias de exposição (p < 0,05), porém a expressão de mRNA da γ-GCS diminuiu significativamente aos 14 dias; a expressão de IL-1 beta no grupo 3 aumentou significativamente aos 7 dias de exposição (p < 0,05) e diminuiu significativamente aos 14 dias. Comparadas ao grupo 3, as expressões do mRNA da GSH e da γ-GCS no grupo 4 aumentaram significativamente com um...

Keratinocyte growth factor, tumor necrosis factor-alpha and interleukin-1 beta gene expression in cultured fibroblasts and keratinocytes from burned patients

Gragnani,Alfredo; Müller,Bruno Rafael; Silva,Ismael Dale Contrim Guerreiro da; Noronha,Samuel Marcos Ribeiro de; Ferreira,Lydia Masako
Fonte: Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia Publicador: Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/08/2013 Português
Relevância na Pesquisa
75.9%
PURPOSE: To evaluate the gene expression of KGF, TNF-alpha and IL-1 beta in skin fibroblasts and keratinocytes cultured from burned patients. METHODS: Three patients with large burns and three patients with small burns, as well as two controls, were included. The cell culture was initiated by the enzymatic method. After extraction and purification of mRNA, qPCR was used to assess the gene expression of KGF, TNF-alpha and IL-1 beta. RESULTS: The expression of KGF was increased on average 220-fold in large burns and 33.33-fold in small burns in fibroblasts, and 11.2-fold in large burns and 3.45-fold in small burns in keratinocytes compared to healthy patients (p<0.05). Expression of TNF-alpha was not observed. IL-1 beta is down-regulated in fibroblasts of burned patients, and much more repressed in small burns (687-fold, p<0.05). In keratinocytes, the repression of IL-1 beta expression occurs in patients with small burns (28-fold), while patients with large burns express this gene intensively (15-fold). CONCLUSIONS: The study showed a quantitative pattern in the expression of KGF gene, which is more expressed according to the size of the burn. TNF-alpha was not expressed. A qualitative pattern in the expression of IL-1 beta gene was demonstrated.

Mechanism of anaemia in rheumatoid arthritis: demonstration of raised interleukin 1 beta concentrations in anaemic patients and of interleukin 1 mediated suppression of normal erythropoiesis and proliferation of human erythroleukaemia (HEL) cells in vitro.

Maury, C P; Andersson, L C; Teppo, A M; Partanen, S; Juvonen, E
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /12/1988 Português
Relevância na Pesquisa
66.06%
The pathogenesis of the anaemia associated with rheumatoid disease is unclear. It has previously been shown that the degree of the anaemia correlates with the severity of the inflammatory disease and that serum from patients with arthritis inhibits erythropoiesis. This study was designed to examine whether interleukin 1 could be a mediator of the anaemia in rheumatoid arthritis. Radioimmunoassay of interleukin 1 beta in serum showed that patients with rheumatoid arthritis and associated anaemia had significantly higher interleukin 1 beta concentrations than patients with rheumatoid arthritis without anaemia. Pure recombinant human interleukin 1 alpha and interleukin 1 beta, in concentration ranges similar to those found in the arthritic patients, markedly suppressed the colony formation of the erythroid, but not the granulocyte-macrophage progenitor cells in cultures of normal bone marrow. Natural human interleukin 1 and recombinant interleukin 1 beta, but not interleukin 1 alpha, suppressed in a dose dependent manner the proliferation of the human erythroleukaemia cell line (HEL) in cultures, suggesting that the interleukin 1 effect is a direct one. The results show that interleukin 1 is a humoral inhibitor of erythropoiesis and suggests that interleukin 1 is involved in the development of anaemia in association with rheumatoid arthritis.

Expression of interleukin-1 alpha, interleukin-1 beta and interleukin-6 in chronic B lymphocytic leukaemia (B-CLL) cells from patients at different stages of disease progression.

Aguilar-Santelises, M; Magnusson, R; Svenson, S B; Loftenius, A; Andersson, B; Mellstedt, H; Jondal, M
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /06/1991 Português
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66.03%
We have previously found that isolated B-CLL cells from progressive disease produce less interleukin-1 beta (IL-1 beta) as compared with cells from patients with indolent disease. Here we extend that finding to include measurements of IL-1 beta mRNA and secretion of IL-1 alpha and interleukin-6 (IL-6). As before, a lower production of IL-1 beta was found in cells from progressive disease. IL-6 was produced by cells from patients at all stages, with a tendency to follow the IL-1 beta production. Low secretion of IL-1 alpha was noted. When viable cells were permeabilized and analysed at the single cell level with monoclonal antibodies, most B-CLL cells were found to contain IL-1 alpha. A minor fraction of non-permeabilized cells expressed IL-1 alpha at the cell membrane. However, only small fractions of cells were positive for intracellular IL-1 beta (less than 1%) and almost no IL-6-positive cells were found. We conclude that either IL-1 beta and IL-6 are produced by a minor population of undefined cells, or that a more sensitive in situ method is needed to detect production of these cytokines in B-CLL cells. The possible biological significance of secreted, and membrane-expressed helper factors in B-CLL is discussed.

Early expression and cellular localization of proinflammatory cytokines interleukin-1[beta], interleukin-6, and tumor necrosis factor-[alpha] in human traumatic spinal cord injury

Yang, L.; Blumbergs, P.; Jones, N.; Manavis, J.; Sarvestani, G.; Ghabriel, M.
Fonte: Lippincott Williams & Wilkins Publicador: Lippincott Williams & Wilkins
Tipo: Artigo de Revista Científica
Publicado em //2004 Português
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96.07%
Study Design. Post-traumatic inflammatory response was studied in 11 human cases of acute spinal cord contusion injury. Objectives. To examine the inflammatory cellular response and the immunocytochemical expression and localization of interleukin-1[beta], internleukin-6, and tumor necrosis factor-[alpha]in human spinal cord after contusion injury. Summary of Background Data. The post-traumatic inflammatory response plays an important role in secondary injury mechanisms after spinal cord injury, and inter-leukin-1[beta], internleukin-6, and tumor necrosis factor-[alpha] are key inflammatory mediators. Methods. The study group comprised 11 patients with spinal cord contusion injury and 2 normal individuals. Histologic and immunocytochemical assessments were undertaken to evaluate the inflammatory cellular response and the immunoexpression of interleukin-1[beta], internleukin-6, and tumor necrosis factor-[alpha] in the injured human spinal cord. The cellular sources of interleukin-1[beta], internleukin-6, and tumor necrosis factor-[alpha] were elucidated by immunofluorescence double-labeled confocal imaging. Results. Increased immunoreactivity of interleukin-1[beta], internleukin-6, and tumor necrosis factor-[alpha]was detected in neurons 0.5 hour after injury...

Regulation of interleukin-1[Beta] and tumor necrosis factor[alpha] synthesis by fatty acids and eicosanoids / by Gillian Elizabeth Caughey.

Caughey, Gillian Elizabeth
Fonte: Universidade de Adelaide Publicador: Universidade de Adelaide
Tipo: Tese de Doutorado Formato: 269444 bytes; application/pdf
Publicado em //1998 Português
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85.82%
Examines the regulation of interleukin-1[Beta] and tumor necrosis factor[alpha] synthesis by fatty acids and eicosanoids by examining the mediator synthesis following dietary fatty acid manipulation; Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 1998; Bibliography: leaves 267-345.; xi, 345, [61] leaves : ill. ; 30 cm.

The Interleukin 1 Beta (IL1B) Gene Is Associated with Failure to Achieve Remission and Impaired Emotion Processing in Major Depression

Baune, B.; Dannlowski, U.; Domschke, K.; Janssen, D.; Jordan, M.; Ohrmann, P.; Bauer, J.; Biros, E.; Arolt, V.; Kugel, H.; Baxter, A.; Suslow, T.
Fonte: Elsevier Science Inc Publicador: Elsevier Science Inc
Tipo: Artigo de Revista Científica
Publicado em //2010 Português
Relevância na Pesquisa
95.89%
Background: Accumulating evidence suggests the involvement of inflammatory processes and cytokines in particular in the pathophysiology of major depression (MDD) and resistance to antidepressant treatment. Furthermore, amygdala and anterior cingulate cortex (ACC) responsiveness to emotional stimuli has been suggested as a predictor of treatment response. This study investigated the association between genetic variants of the interleukin 1 beta (IL1B) gene and amygdala and ACC responsiveness to emotional stimuli and response to antidepressant treatment. Methods: In this analysis, 256 Caucasian patients with MDD (145 women, 111 men) were genotyped for variants rs16944, rs1143643, and rs1143634 in the IL1B gene (2q14). Response to antidepressant treatment over 6 weeks was defined as remission (≤ 7 on the Hamilton Rating Scale for Depression–21-question) and response (>50% decrease on Hamilton Rating Scale for Depression–21-question). Brain activity under visual presentation of emotional faces was assessed in a subsample of 32 depressed patients by means of functional magnetic resonance imaging at 3 T. Results: Pharmacogenetic analyses show significant associations of the GG genotypes of single nucleotide polymorphisms (SNPs) rs16944 (odds ratio = 1.74; 95% confidence interval 1.2–4.3) and rs1143643 (odds ratio = 3.1; 95% confidence interval 1.3–7.8) (compared with the AA genotype) with nonremission after 6 weeks. The imaging analyses show that the number of G-alleles in both SNPs (rs16944 and rs1143643) was associated with reduced responsiveness of the amygdala and ACC to emotional stimulation. Conclusions: The present study suggests a negative effect of the IL1B gene on pharmacological response and amygdala and ACC function involving the same genotypes of two SNPs (rs16944...

CNS immune signalling and drug addiction: the role of interleukin-1 beta.

Liu, Liang
Fonte: Universidade de Adelaide Publicador: Universidade de Adelaide
Tipo: Tese de Doutorado
Publicado em //2011 Português
Relevância na Pesquisa
95.91%
Opioid and alcohol dependencies are significant public health problems worldwide. The causes of drug dependence are complex, comprising both genetic and environmental factors. Recent evidence from animal models has shown that opioid-/alcohol-induced proinflammation within the central nervous system (CNS) plays a contributing role in the development of dependence. Proinflammatory cytokines, such as interleukin-1 beta (IL-1β), may be involved in the development of opioid/alcohol dependence. Thus, genetic polymorphisms in the proinflammatory cytokine genes that alter their expression and/or function may alter the risk of dependence in humans. Previously, genetic polymorphisms in two genes, IL-1B and IL-1RN, which encode for IL-1β and IL-1 receptor antagonist (IL-1Ra), respectively, were shown to be associated with altered risk of alcohol dependence. However, this has yet to be examined in an opioid dependent population. Therefore, the first major aim of this thesis was to examine the possible association between genetic variability of IL-1B and IL-1RN in opioid dependent and healthy control populations. In order to confirm the previous study within the Australian context, this thesis also examined the variability of the IL-1B and IL-1RN genetic polymorphisms in an Australian alcohol dependent population. Genomic DNA from opioid dependent subjects (n = 60)...

HIV-1 induces NALP3-inflammasome expression and interleukin-1 beta secretion in dendritic cells from healthy individuals but not from HIV-positive patients

Pontillo, Alessandra; Silva, Lais T.; Sumida, Telma Miyuki Oshiro; Finazzo, Claudia; Crovella, Sergio; Duarte, Alberto Jose da Silva
Fonte: LIPPINCOTT WILLIAMS & WILKINS; PHILADELPHIA Publicador: LIPPINCOTT WILLIAMS & WILKINS; PHILADELPHIA
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
95.93%
Objective: NALP3-inflammasome is an innate mechanism, alternative to type-1 interferon, which is able to recognize nucleic acids and viruses in the cytoplasm and to induce pro-inflammatory response. Here, we hypothesized the involvement of inflammasome in the early defense against HIV-1 and in the full maturation of dendritic cells: for this, we evaluated the response of dendritic cells pulsed with HIV-1 in terms of inflammasome activation in healthy donors. Moreover, inflammasome response to HIV was evaluated in HIV-infected individuals. Design and methods: Monocyte-derived dendritic cells isolated from 20 healthy individuals (HC-DC) and 20 HIV-1-infected patients (HIV-DC) were pulsed with alditrithiol-2-inactivated HIV-1. We then analyzed inflammasome genes expression and interleukin-1 beta (IL-1 beta) secretion. Results: In HC-DC, HIV-1 induced higher NLRP3/NALP3 mRNA expression compared with other inflammasome genes such as NALP1/NLRP1 or IPAF/NLRC4 (P < 0.001). This augmented expression was accompanied by CASP1-increased and IL1B-increased mRNA levels and by a significant increment of IL-1b secretion (P < 0.05). Otherwise, HIV-1 failed to activate inflammasome and cytokine production in HIV-DC. HIV-DC showed an increased NLRP3/NALP3 basal expression...

Niveles plasmáticos de citoquinas IL-1, IL2 e IL-4 en niños diabéticos tipo 1 de diagnóstico reciente y su asociación con anticuerpos pancreáticos; Plasma levels of interleukin-1 beta, interleukin-2 and interleukin-4 in recently diagnosed type 1 diabetic children and their association with 9-pancreatic autoantibodies

Carrasco Piña, Elena; Ángel Badillo, Bárbara Karen; Albala Brevis, Cecilia Hortensia; Oyarzún, Amaya; Santos, José Luis; Pérez Bravo, Francisco
Fonte: SOC MEDICA SANTIAGO Publicador: SOC MEDICA SANTIAGO
Tipo: Artículo de revista
Português
Relevância na Pesquisa
66.02%
Background: Type 1 diabetes is an organ specific autoimmune disease whose incidence is increasing worldwide. A functional imbalance in cytokine production resulting in dominance of T helper (Th1) over Th2-type response has been suggested to play a critical role in the pathogenesis of type 1 diabetes. Aim: To measure serum concentrations of interleukin (IL)-1 beta, IL-2 and IL-4 in children with recently diagnosed type 1 diabetes and to evaluate the autoimmune response measuring glutamic acid decarboxylase (GAD65) and tyrosine phosphatase like (IA-2) autoantibodies. Patients and Methods: 120 diabetic children and 118 age and gender matched control children, were recruited for this study. Circulating levels of IL-1 beta IL-2 and IL-4 were measured by ELISA. GAD65 and IA-2 were measured by RIA. Results: Circulating levels of IL-1 beta were elevated in type 1 diabetic children as compared to the control group (9.3 +/- 7.3 and 4.9 +/- 3.8 mu g/ml respectively, p=0,01). Serum concentration of IL-2 was also higher diabetic patients (19.8 +/- 13.1 and 11.3 +/- 9.1 pg/ml respectively, p=0,01). No differences in serum IL-4 were observed between diabetics and control. Diabetic children with one or two positive autoantibodies (IA-2 and/or GAD65) had significantly higher levels of IL-1 beta and IL-2 and lower levels of IL-4 than diabetic children without positive autoantibodies. High concentrations of IL-1 beta associated with an early onset of the disease. Conclusions: High levels of IL-1 beta and IL-2 were found in diabetic children with recent diagnosis of the disease. Diabetics with positive antibodies against GAD65 and IA-2 had higher levels of IL-1 beta...