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Amniotic Fluid Interleukin-1 Beta and Interleukin-6, but not Interleukin-8 Correlate with Microbial Invasion of the Amniotic Cavity in Preterm Labor

Marconi, Camila; Andrade Ramos, Bruna Ribeiro de; Peraçoli, José Carlos; Donders, Gilbert G. G.; Silva, Marcia da
Fonte: Wiley-Blackwell Publicador: Wiley-Blackwell
Tipo: Artigo de Revista Científica Formato: 549-556
Português
Relevância na Pesquisa
55.93%
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP); Processo FAPESP: 07/50726-7; Processo FAPESP: 07/52758-3; ProblemWe compared the frequency of intra-amniotic infection in preterm labor (PL) with women not in labor, and correlated infection with amniotic fluid (AF) cytokines. Detailed identification of species, especially mycoplasmata, was tried to improve our understanding of the pathogenesis of PL.Method of studyAF from 20 women with PL and 20 controls were evaluated. Infection was detected by PCR for Mycoplasma hominis, Ureaplasma urealyticum and 16S rRNA bacterial gene, which was cloned and sequenced for bacterial identification. Interleukin (IL)-1 beta, IL-6, IL-8 and tumor necrosis factor (TNF)-alpha levels were measured by ELISA.ResultsFrequency of intra-amniotic infection is higher in PL (40.0%). Sequencing-based method identified Bacteroides fragilis, Prevotella bivia and Leptotrichia amnionii, in addition to Mycoplasma species detected by PCR. AF infection correlated with increased IL-1 beta and IL-6 levels.ConclusionThe frequency of intra-amniotic infection, especially M. hominis, in PL women who delivered with 7 days, is high and correlates with high IL-1 beta and IL-6 levels, but not IL-8.

Depletion of endogenous interleukin-10 augments interleukin-1 beta secretion by Mycobacterium bovis BCG-reactive human cells.

Méndez-Samperio, P; Garcia-Martinez, E; Hernandez-Garay, M; Solis-Cardona, M
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /03/1997 Português
Relevância na Pesquisa
55.93%
In this study, we found evidence that the interleukin-10 (IL-10) protein is functionally relevant in Mycobacterium bovis BCG-induced cytokine synthesis, as neutralization of endogenously synthesized IL-10 in human cells activated with BCG resulted in a two- to threefold increase in the level of IL-1 beta. When exogenous recombinant human IL-10 was added to human mononuclear cells, a significant reduction of BCG-induced IL-1 beta secretion was observed. This inhibitory effect was not attributed to a cytotoxic effect, since trypan blue exclusion studies indicated no loss of cell viability in the presence of IL-10, and it was specific, as it was completely abolished in the presence of anti-IL-10 neutralizing monoclonal antibody while an irrelevant antibody used as a control had no effect. Taken together, these are the first studies that demonstrate that the depletion of endogenous IL-10 via anti-IL-10 antibody results in a very significantly enhanced BCG-induced IL-1 beta secretion and that the addition of exogenous IL-10 to human mononuclear cells stimulated with BCG inhibits IL-1 beta production. Further experimental work is needed to determine if the neutralization of IL-10 activity via anti-IL-10 antibody indeed enhances cytokine synthesis in vivo. However...

Human immunodeficiency virus does not induce interleukin-1, interleukin-6, or tumor necrosis factor in mononuclear cells.

Molina, J M; Scadden, D T; Amirault, C; Woon, A; Vannier, E; Dinarello, C A; Groopman, J E
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /06/1990 Português
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55.94%
The production of interleukin-1 beta (IL-1 beta), IL-6, and tumor necrosis factor alpha (TNF-alpha) by fresh peripheral blood mononuclear cells was evaluated after exposure to human immunodeficiency virus (HIV) or purified recombinant HIV-1 envelope glycoprotein (rgp120). To exclude the role of contaminating endotoxin in this study, all media were subjected to ultrafiltration and reagents contained less than 25 pg of endotoxin per ml by Limulus assay. Under endotoxin-free conditions, no increases in IL-1 beta, IL-6, or TNF-alpha mRNA or protein were detectable in cell cultures exposed to HIV-1, HIV-2, or rgp120 (0.1 to 10 micrograms/ml), as compared with cytokine levels in mock-exposed cultures. However, concentrations of endotoxin (lipopolysaccharide) as low as 0.5 ng/ml induced significant production of mRNA and protein for these three cytokines. Preincubation of mononuclear cells with "shake" HIV-1 preparations and also mock-infected shake preparations prior to lipopolysaccharide stimulation resulted in a two- to threefold increase in IL-1 beta and TNF-alpha production. This priming effect was not observed with rgp120 (0.1 to 10 micrograms/ml) or standard HIV-1 or mock-infected supernatants, suggesting the presence of biologically active material independent of virus in the shake preparations. Our studies indicate that...

Provocation of pulmonary vascular endothelial injury in rabbits by human recombinant interleukin-1 beta.

Goldblum, S E; Yoneda, K; Cohen, D A; McClain, C J
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /09/1988 Português
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Interleukin-1 (IL-1) mediates components of the acute-phase response, stimulates granulocyte metabolism, and induces endothelial cell surface changes. We studied the effects of human recombinant IL-1 beta (rIL-1 beta) or rIL-1 alpha on circulating granulocytes, their sequestration within the pulmonary microvasculature, pulmonary edema formation, and changes in pulmonary vascular permeability to 125I-labeled albumin. rIL-1 beta administration induced significant (P less than 0.03) but transient granulocytopenia followed by significant (P less than 0.04) neutrophilia and significant (P less than 0.04) pulmonary leukostasis compared with saline-infused rabbits. Rabbits preinfused with 125I-labeled rabbit serum albumin and administered saline, rIL-1 beta, or rIL-1 alpha were sacrificed, and lung wet/dry weight ratios and bronchoalveolar lavage fluid and plasma 125I activities determined. Both rIL-1 beta and rIL-1 alpha increased lung wet/dry weight ratios (P less than 0.025 and P less than 0.01, respectively) compared with saline controls. rIL-1 beta increased bronchoalveolar lavage fluid/plasma 125I radioactivity ratios (P less than 0.025). Electron microscopic analysis of lung sections obtained from rIL-1 beta-infused animals demonstrated endothelial injury...

Identification of a monocyte specific pre-interleukin 1 beta convertase activity.

Kostura, M J; Tocci, M J; Limjuco, G; Chin, J; Cameron, P; Hillman, A G; Chartrain, N A; Schmidt, J A
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /07/1989 Português
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Interleukin 1 (IL-1) is a lymphokine secreted by monocytes in response to a variety of inflammatory stimuli. IL-1 beta, the predominant form of IL-1 produced by human monocytes, is synthesized as an inactive precursor of 31 kDa and is cleaved at Asp116-Ala117 to yield a 17.5-kDa extracellular form. The exact cellular site of cleavage and mechanism of secretion is at present unknown. We have prepared cell-free postnuclear extracts from freshly isolated human monocytes as well as THP.1 cells, a human monocyte-like cell line, and various blood lymphocytes and fibroblast cell lines. Using pre-IL-1 beta synthesized by in vitro transcription and translation, we have shown that only extracts derived from human monocytes and THP.1 cells were capable of cleaving precursor IL-1 beta to authentic mature IL-1 beta. Subcellular fractionation of the extracts suggested that the processing activity is found in the cytosol of monocytes or monocyte-like cell lines. The cleavage product of this protease is identical to authentic IL-1 beta as shown by mobility on SDS/PAGE and amino acid sequence analysis of the [3H]leucine-labeled product. The cleavage product is also capable of binding to the IL-1 receptor found on fibroblast membranes. Finally, mutation of Asp116----Ala116 rendered the IL-1 beta precursor resistant to cleavage by the processing activity. We conclude that a protease activity found only in monocytes will specifically process IL-1 beta to an active form.

Identification of a high-affinity receptor for interleukin 1 alpha and interleukin 1 beta on cultured human rheumatoid synovial cells.

Chin, J; Rupp, E; Cameron, P M; MacNaul, K L; Lotke, P A; Tocci, M J; Schmidt, J A; Bayne, E K
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /08/1988 Português
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55.94%
In this report the binding of recombinant human interleukins 1 alpha and 1 beta (rIL-1 alpha and rIL-1 beta) to primary cultures of human rheumatoid synovial cells is measured and compared to the concentrations of these mediators required for stimulation of PGE2 production by these same cells. The average concentration of IL-1 alpha required for half-maximal stimulation of PGE2 was 4.6 +/- 1.5 pM (+/- SEM) (n = 6), whereas for IL-1 beta half-maximal stimulation was observed at a concentration of 1.3 +/- 0.24 pM (n = 6). Both direct and competitive binding experiments were performed. In direct binding experiments, IL-1 alpha bound with a Kd of 66 pM (n = 1), while IL-1 beta bound with a Kd of 4 pM (n = 2). In competitive binding experiments, IL-1 alpha inhibited binding of 125I-IL-1 alpha with a Ki of 33-36 pM (n = 2) and binding of 125I-IL-1 beta with a Ki of 51-63 pM (n = 2). IL-1 beta inhibited binding of 125I-IL-1 alpha with a Ki of 2-3 pM (n = 2) and binding of 125I-IL-1 beta with a Ki of 7 pM (n = 2). The binding data were best fit by a model specifying a single class of receptors with homogeneous affinity for either IL-1 alpha or IL-1 beta and with an abundance of 3,000-14,000 sites per cell. Autoradiography showed that the vast majority of the synoviocytes within the cultures possessed IL-1 receptors. Comparison of biological response curves with the binding curves indicates that the observed receptors exhibit sufficiently high affinity to mediate the response of human synoviocytes to low picomolar concentrations of IL-1 alpha and IL-1 beta.

Stimulation of glycosaminoglycan synthesis in cultured human dermal fibroblasts by interleukin 1. Induction of hyaluronic acid synthesis by natural and recombinant interleukin 1s and synthetic interleukin 1 beta peptide 163-171.

Postlethwaite, A E; Smith, G N; Lachman, L B; Endres, R O; Poppleton, H M; Hasty, K A; Seyer, J M; Kang, A H
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /02/1989 Português
Relevância na Pesquisa
55.95%
Hyaluronic acid (HA) is believed to play a critical role in wound healing and in morphogenesis. Factors controlling the production of HA by fibroblasts in normal and pathological states are not completely understood. In this report we have observed that natural human interleukin (IL-1)1 beta and human recombinant (hrIL)-1 alpha and beta are potent stimulators of HA production by fibroblasts in vitro. Hyaluronic acid is the major species of glycosaminoglycan (GAG) stimulated by IL-1 in fibroblasts. PGE2 does not appear to be involved directly in this IL-1 effect on fibroblasts, but stimulation of HA production by IL-1 is dependent on protein synthesis. The synthetic human IL-1 beta peptide 163-171 (Val-Gln-Gly-Glu-Glu-Ser-Asn-Asp-Lys), which has been previously shown to stimulate thymocyte proliferation but not fibroblast PGE2 production, is also able to stimulate fibroblast HA production. The synthesis and secretion of IL-1 by mononuclear phagocytes at sites of inflammation and immune reactions in vivo could potentially serve as a signal for fibroblasts to synthesize HA, which in turn could serve to facilitate and modulate reparative and immune processes by virtue of its ability to alter cell-cell, cell matrix, and cell-membrane receptor interactions.

Live Borrelia burgdorferi preferentially activate interleukin-1 beta gene expression and protein synthesis over the interleukin-1 receptor antagonist.

Miller, L C; Isa, S; Vannier, E; Georgilis, K; Steere, A C; Dinarello, C A
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /09/1992 Português
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55.95%
Lyme arthritis is one of the few forms of chronic arthritis in which the cause is known with certainty. Because cytokines are thought to contribute to the pathogenesis of chronic arthritis, we investigated the effect of the Lyme disease spirochete, Borrelia burgdorferi, on the gene expression and synthesis of IL-1 beta and the IL-1 receptor antagonist (IL-1ra) in human peripheral blood mononuclear cells. Live B. burgdorferi induced fivefold more IL-1 beta than IL-1 alpha and sevenfold more IL-1 beta than IL-1ra; LPS or sonicated B. burgdorferi induced similar amounts of all three cytokines. This preferential induction of IL-1 beta was most dramatic in response to a low passage, virulent preparation of B. burgdorferi vs. three high passage avirulent strains. No difference in induction of IL-1ra was seen between these strains. The marked induction of IL-1 beta was partially diminished by heat-treatment and abrogated by sonication; IL-1ra was not affected. This suggested that a membrane component(s) accounted for the preferential induction of IL-1 beta. However, recombinant outer surface protein beta induced little IL-1 beta. By 4 h after stimulation, B. burgdorferi induced sixfold more IL-1 beta protein than LPS. In contrast to LPS-induced IL-1 beta mRNA which reached maximal accumulation after 3 h...

Potassium-inhibited processing of IL-1 beta in human monocytes.

Walev, I; Reske, K; Palmer, M; Valeva, A; Bhakdi, S
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em 18/04/1995 Português
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55.94%
Agents that deplete cells of K+ without grossly disrupting the plasma membrane were found to stimulate the cleavage of pro-interleukin (IL)-1 beta to mature IL-1 beta. Agents examined in this study included staphylococcal alpha-toxin and gramicidin, both of which selectively permeabilize plasma membranes for monovalent ions, the ionophores nigericin and valinomycin, and the Na+/K+ ATPase inhibitor ouabain. K+ depletion by brief hypotonic shock also triggered processing of pro-IL-1 beta. The central role of K+ depletion for inducing IL-1 beta maturation was demonstrated in cells permeabilized with alpha-toxin: processing of pro-IL-1 beta was totally blocked when cells were suspended in medium that contained high K+, but could be induced by replacing extracellular K+ with Na+, choline+ or sucrose. To test whether K+ flux might also be important in physiological situations, monocytes were stimulated with lipopolysaccharide (LPS) for 1-2 h to trigger pro-IL-1 beta synthesis, and transferred to K(+)-rich medium. This maneuver totally suppressed IL-1 beta maturation. Even after 16 h, however, removal of K+ from the medium resulted in rapid processing and export of IL-1 beta. Ongoing export of mature IL-1 beta from cells stimulated with LPS for 2-6 h could also be arrested by transfer to K(+)-rich medium. Moreover...

Concentration of fetal plasma and amniotic fluid interleukin-1 in pregnancies complicated by preterm prelabour amniorrhexis.

Carroll, S G; Abbas, A; Ville, Y; Meher-Homji, N; Nicolaides, K H
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /04/1995 Português
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55.92%
AIMS--To determine interleukin-1 beta (IL-1 beta) concentration in fetal and maternal plasma and amniotic fluid from pregnancies complicated by preterm prelabour amniorrhexis and to define the relation of this cytokine to intrauterine infection and the onset of labour. METHODS--Cross-sectional study of 23 pregnancies complicated by preterm prelabour amniorrhexis. Enzyme linked immunoassay was used to measure IL-1 beta concentration in fetal and maternal plasma and amniotic fluid. In each case, fetal blood and amniotic fluid were cultured for micro-organisms. RESULTS--In pregnancies with positive fetal blood and/or amniotic fluid cultures, plasma and amniotic fluid concentrations of IL-1 beta were higher and the interval between amniorrhexis and onset of labour was shorter than in the non-infected group. There were no significant associations between fetal plasma IL-1 beta and maternal plasma or amniotic fluid IL-1 beta concentrations, fetal leucocyte count or the interval between amniorrhexis and the onset of labour. CONCLUSIONS--These findings suggest that although intrauterine infection is associated with increased IL-1 beta concentrations in fetal plasma and amniotic fluid, there is no significant association between the concentration of IL-1 beta and the interval between amniorrhexis and the onset of labour.

A novel secretory pathway for interleukin-1 beta, a protein lacking a signal sequence.

Rubartelli, A; Cozzolino, F; Talio, M; Sitia, R
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /05/1990 Português
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55.93%
Interleukin 1 (IL-1) is a major soluble mediator of inflammation. Two human IL-1 genes, alpha and beta, have been isolated, which encode polypeptides with only 20-30% amino acid sequence homology. Unlike most secreted proteins, the two cytokines do not have a signal sequence, an unexpected finding in view of their biological role. Here we show that IL-1 beta is actively secreted by activated human monocytes via a pathway of secretion different from the classical endoplasmic reticulum--Golgi route. Drugs which block the intracellular transport of IL-6, of tumour necrosis factor alpha and of other secretory proteins do not inhibit secretion of IL-1 beta. Secretion of IL-1 beta is blocked by methylamine, low temperature or serum free medium, and is increased by raising the culture temperature to 42 degrees C or by the presence of calcium ionophores, brefeldin A, monensin, dinitrophenol or carbonyl cyanide chlorophenylhydrazone. IL-1 beta is contained in part within intracellular vesicles which protect it from protease digestion. In U937 cells large amounts of IL-1 beta are made but none is secreted. In these cells IL-1 beta is not found in the vesicular fraction, and all the protein is accessible to protease digestion. This suggests that intracellular vesicles that contain IL-1 beta are part of the protein secretory pathway. We conclude that IL-1 beta is released by activated monocytes via a novel mechanism of secretion which may involve translocation of intracellular membranes and is increased by stress conditions.

Possible involvement of glucocorticoids in the modulation of interleukin-1-induced cardiovascular responses in rats.

Watanabe, T; Tan, N; Saiki, Y; Makisumi, T; Nakamura, S
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em 15/02/1996 Português
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1. In freely moving rats, we investigated whether glucocorticoids modulate the cardiovascular responses to intraperitoneal (I.P.) injection of interleukin-1 beta (IL-1 beta). 2. A lower dose of IL-1 beta (1 microgram kg-1, I.P.) induced monophasic increases, and a higher dose (10 micrograms kg-1, I.P.) induced biphasic increases in both blood pressure and heart rate. Plasma concentration of corticosterone increased significantly after injection of IL-1 beta (10 micrograms kg-1). 3. Systemic pretreatment with an exogenous glucocorticoid, dexamethasone (DEX; 0.5 mg kg-1) reduced the monophasic pressor response, the first phase of the biphasic pressor response and also the initial tachycardia. By contrast, the second phase of the biphasic pressor response was enhanced. 4. After bilateral adrenalectomy, the IL-1 beta (10 micrograms kg-1)-induced pressor effect was reduced; it was restored by treatment with DEX (0.5 mg kg-1). The heart rate response was enhanced in adrenalectomized (ADX) rats; this enhancement was attenuated by DEX. 5. IL-1 beta (10 micrograms kg-1)-induced increases in plasma noradrenaline (NA) were suppressed in intact rats pretreated with DEX (0.5 mg kg-1). The IL-1 beta-induced NA response was greater in ADX rats than in sham-ADX rats. 6. We suggest that glucocorticoids are an important modulator of cardiovascular responses induced in rats by systemically administered IL-1 beta.

Cross-linking of the high-affinity IgE receptor induces the expression of cyclo-oxygenase 2 and attendant prostaglandin generation requiring interleukin 10 and interleukin 1 beta in mouse cultured mast cells.

Ashraf, M; Murakami, M; Kudo, I
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em 15/12/1996 Português
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When mouse bone marrow-derived mast cells (BMMC) developed in interleukin (IL)-3 were activated with IgE and antigen (IgE/antigen) in the presence of both IL-10 and IL-1 beta, two sequential phases of prostaglandin (PG)D2 generation were elicited, in which the first phase occurred by 1 h and the second phase from 2 to 10 h. The delayed phase of PGD2 generation was accompanied by a marked induction of cyclo-oxygenase (COX)-2 mRNA, which reached a peak at 1-2 h, followed by that of its protein from 2-10 h, with a peak at 5 h. The immediate phase of PGD2 generation was completely abrogated by the irreversible inhibition of pre-existing COX-1 by aspirin pretreatment, whereas the delayed phase of PGD2 generation was almost undetectable in the presence of the COX-2 inhibitor NS-398. A detailed analysis of the individual effects of IgE/antigen, IL-10 and IL-1 beta on COX-2 expression revealed that IgE/antigen and IL-10 each initiated and stabilized COX-2 mRNA expression, leading to an increase in the expression of its protein. Conversely, IL-1 beta stabilized the COX-2 protein without affecting its mRNA level. The induction of COX-2 by IgE/antigen with IL-10 and IL-1 beta preceded the induction of transcripts for endogenous cytokines such as IL-6...

Role of neutrophils in a rat model of gastric ulcer recurrence caused by interleukin-1 beta.

Watanabe, T.; Arakawa, T.; Fukuda, T.; Higuchi, K.; Kobayashi, K.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /03/1997 Português
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55.94%
The production of several cytokines such as interleukin (IL)-1 in gastric mucosa is increased in subjects infected with Helicobacter pylori, a bacterium associated with ulcer recurrence. This study was performed to determine whether the administration of IL-1 beta can cause recurrence of gastric ulcers in rats. Rats with healed ulcers received an injection of IL-1 beta (0.01 to 1 microgram/kg) or vehicle alone. Some rats received an injection of antiserum to rat neutrophils at the same time as 1 microgram/kg IL-1 beta or an injection of monoclonal antibodies against adhesion molecules (anti-intercellular adhesion molecule-1, anti-CD11a, and anti-CD11b) at 0, 12, and 24 hours after the initial injection. At this dose of IL-1 beta, the numbers of neutrophils and monocytes/macrophages infiltrating the scarred mucosa were higher at 12 and 24 hours than without injection of IL-1 beta. By 48 hours, seven of the eight bealed ulcers in the group treated with 1 microgram/kg IL-1 beta had recurred, as had one of the seven healed ulcers in the group given 0.1 microgram/kg IL-1 beta. No recurrence was found in the rats treated with 0.01 microgram/kg IL-1 beta or vehicle alone. Treatment with antiserum to neutrophils or antibodies to adhesion molecules inhibited both neutrophil infiltration into the scarred mucosa and the ulcer recurrence caused by IL-1 beta. These findings suggest possible mechanisms of recurrence of human peptic ulcers.

Human peritoneal mesothelial cells synthesize interleukin-8. Synergistic induction by interleukin-1 beta and tumor necrosis factor-alpha.

Topley, N.; Brown, Z.; Jörres, A.; Westwick, J.; Davies, M.; Coles, G. A.; Williams, J. D.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /06/1993 Português
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The present study demonstrates the synthesis and secretion of the neutrophil-activating peptide/interleukin-8 (IL-8) by cultured human peritoneal mesothelial cells (HPMC) and examines the regulation of its production by other cytokines. Unstimulated HPMC under growth-arrested conditions released IL-8 in a constitutive and time-dependent manner. Stimulation of HPMC with IL-1 beta or TNF-alpha resulted in a time- and dose-dependent IL-8 generation; after 24 hours the levels induced by IL-1 beta and TNF-alpha (both at 1000 pg/ml) were (mean +/- SEM, n = 5) 101 +/- 26.6 (z = 2.023; P < 0.01) and 35 +/- 8.09 (z = 2.023; P < 0.01) respectively. This release was inhibited following coincubation with the relevant anti-cytokine antibody or preincubation with either cycloheximide or actinomycin D. Treatment of HPMC with IL-1 beta or TNF-alpha resulted in increased levels of IL-8-specific mRNA. Stimulation of HPMC with combinations of IL-1 beta and TNF-alpha resulted in a synergistic increase in IL-8 release. This effect was significant at combined doses of IL-1 beta (50 pg/ml) and TNF-alpha (500 pg/ml) and above, when the release of IL-8 was 88 +/- 27% above the additive IL-8 release values (z = 2.201; P < 0.01). Western blot analysis using specific anti-IL-8 antibody demonstrated the presence of two major immunoreactive bands between 9 and 10 kd...

Purification and characterization of a novel soluble receptor for interleukin 1

Fonte: The Rockefeller University Press Publicador: The Rockefeller University Press
Tipo: Artigo de Revista Científica
Publicado em 01/11/1991 Português
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55.93%
Affinity chromatography and reverse-phase high-performance liquid chromatography was used to purify a soluble interleukin 1 beta (IL-1 beta) specific binding protein from the supernatant of a human B cell line, Raji. The purified protein specifically bound 125I IL-1 beta forming a 60-kD complex in nonreducing conditions and a 70-kD complex in reducing conditions. Binding was found to be displaceable by mature human and murine IL-1 beta and human 31-kD IL-1 beta propeptide, but not displaceable by human and murine IL-1 alpha or human IL-1 receptor (IL-1R) antagonist. Ligand blotting revealed a 47-kD molecule that specifically bound IL-1 beta. Measurement of binding affinity of the cell surface Raji IL-1R (Kd = 2.2 nm) and the Raji soluble (s)IL-1R (Kd = 2.7 nm) demonstrated a similar affinity for 125I IL-1 beta. Purified sIL-1R inhibited binding of IL-1 beta to cell lines with both type I (80 kD) and type II (65 kD) IL-1Rs, but did not interfere with IL-1 alpha binding. This natural sIL-1R may function as an important regulatory molecule of IL-1 beta in vivo.

Identification of a high-affinity receptor for native human interleukin 1 beta and interleukin 1 alpha on normal human lung fibroblasts

Fonte: The Rockefeller University Press Publicador: The Rockefeller University Press
Tipo: Artigo de Revista Científica
Publicado em 01/01/1987 Português
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55.93%
Native human IL-1 beta and IL-1 alpha stimulated prostaglandin E2 secretion by human embryonic lung fibroblasts at half-maximal concentrations of 3 +/- 1.2 pM (+/- SEM) and 10 +/- 2.3 pM, respectively. In contrast to the 20-50-fold lower affinities previously found for IL-1-R on 3T3 cells as well as murine and human lymphoblastoid lines, monoiodo 125I-IL-1 beta bound to normal human fibroblasts with a Kd of 8.4 +/- 4.1 pM in direct binding experiments, and with a Ki of 11.2 +/- 2.8 pM in competitive binding experiments. IL- 1 alpha bound to the receptor identified by 125I-IL-1 beta with a Ki of 50 +/- 18 pM. The receptor exhibited homogeneous affinity for IL-1 beta or IL-1 alpha. The receptor did not recognize IL-2, IFN-gamma, tumor necrosis factor alpha, a functionally related monokine, or bovine acidic fibroblast growth factor, a structurally related mediator. Comparison of the biological response curves and binding curves obtained for IL-1 alpha and IL-1 beta showed that they were parallel and that 10-15% occupancy of the estimated 3,000 sites by either species of IL-1 was sufficient to give half-maximal stimulation of prostaglandin E2 secretion. Thus, the amount of apparent signal amplification observed on fibroblasts was considerably lower than the 100-100...

Cytokine regulation of syndecan-1 and -2 gene expression in human periodontal fibroblasts and osteoblasts

Worapamorn, W.; Tam, S.; Li, H.; Haase, H.; Bartold, P.
Fonte: Munksgaard Int Publ Ltd Publicador: Munksgaard Int Publ Ltd
Tipo: Artigo de Revista Científica
Publicado em //2002 Português
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55.95%
Cell-surface proteoglycans participate in several biological functions including interactions with a variety of growth factors and cytokines. Regulation of syndecan-1 and -2 gene expression was investigated in human periodontal ligament fibroblasts (PDLF), osteoblasts (OB) and gingival fibroblasts (GF), in response to platelet-derived growth factor (PDGF-BB), transforming growth factor (TGF-beta 1), and interleukin (IL-1 beta) by Northern blot analyses. We also compared the effect of PDGF-BB and TGF-beta 1, separately and in combination, in the prolonged presence of IL-1 beta on the expression of both syndecan genes. The results demonstrated that the three cell lines regulated the expression of syndecan-1 and -2 in response to growth factors and cytokines in different manners. These cell lines increased syndecan-1 mRNA levels in response to either PDGF-BB or TGF-beta 1 and decreased levels in response to IL-1 beta. The effect of IL-1 beta on syndecan-1 mRNA synthesis was partially reversed after adding PDGF-BB and TGF-beta 1, separately or in combination, in the presence of IL-1 beta. In contrast, syndecan-2 mRNA level was markedly upregulated in response to either TGF-beta 1 or IL-1 beta in OB when compared with the other two cell lines. However...

The effect on human tumor necrosis factor α and interleukin 1β production of diets enriched in n-3 fatty acids from vegetable oil or fish oil; The effect on human tumor necrosis factor alpha and interleukin 1beta production of diets enriched in n-3 fatty acids from vegetable oil or fish oil

Caughey, G.E.; Mantzioris, E.; Gibson, R.A.; Cleland, L.G.; James, M.J.
Fonte: American Society for Clinical Nutrition Publicador: American Society for Clinical Nutrition
Tipo: Artigo de Revista Científica
Publicado em //1996 Português
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55.95%
The effect of a flaxseed oil-based diet on tumor necrosis factor alpha (TNF alpha) and interleukin 1 beta (IL-1 beta) synthesis was examined in healthy volunteers. Use of flaxseed oil in domestic food preparation for 4 wk inhibited TNF alpha and IL-1 beta production by approximately 30%. Fish-oil supplementation (9 g/d) continued for a further 4 wk; TNF alpha and IL-1 beta synthesis were inhibited by 74% and 80%, respectively. There was a significant inverse exponential relation between TNF alpha or IL-1 beta synthesis and mononuclear cell content of eicosapentaenoic acid (EPA), an n--3 fatty acid derived from ingested EPA (fish oil) or metabolism of ingested alpha-linolenic acid (flaxseed oil). Cytokine production decreased as cellular EPA increased to approximately 1% of total fatty acids. Further increases in EPA content did not result in further decreases in cytokine production. The results indicate that vegetable oils rich in n--3 fatty acids inhibit TNF alpha and IL-1 beta synthesis.; Gillian E Caughey, Evangeline Mantzioris, Robert A Gibson, Leslie G Cleland, and Michael J James

Endotoxin-induced cytokine gene expression in vivo. II. Regulation of tumor necrosis factor and interleukin-1 alpha/beta expression and suppression.

Ulich, T. R.; Guo, K. Z.; Irwin, B.; Remick, D. G.; Davatelis, G. N.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /11/1990 Português
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Tumor necrosis factor alpha (TNF alpha) mRNA is present in a preformed intracellular pool in the spleen, liver, and small bowel of naive rats. Endotoxin (Salmonella typhus lipopolysaccharide) injected intravenously induces little or no increase in whole-organ TNF mRNA levels at 15', 30', 1 degree, 2 degrees, or 4 degrees, whereas serum TNF levels are markedly elevated at 1 and 2 hours. Dexamethasone pretreatment of rats suppresses LPS-induced serum TNF concentrations, but does not suppress TNF mRNA levels in the spleen or bowel. Tachyphylaxis experiments demonstrate that a second injection of endotoxin 2 hours after an initial injection fails to induce a second peak of serum TNF, although TNF mRNA levels in the spleen and bowel remain at the levels found in naive rats. Corynebacterium parvum upregulates endotoxin-induced serum TNF release and intravenous injection of IL-1 induces the release of serum TNF but neither alters whole-organ TNF mRNA levels. Interleukin-1 alpha (IL-1 alpha) mRNA was not constitutively detected in whole-organ RNA preparations of the spleen, liver, and small bowel of naive rats. Endotoxin induces IL-1 alpha mRNA most easily appreciated in the spleen beginning at 1 hour, peaking at 2 to 4 hours, and disappearing by 6 hours. Interleukin-1 beta (IL-1 beta) mRNA was not constitutively detected in the organs examined or was present in small amounts. Endotoxin induces IL-1 beta mRNA beginning at 0.5 hours...