Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The B9 assay is known to be a specific and sensitive assay for the estimation of interleukin-6 activity. This assay was found to be compromised by lipopolysaccharide in concentrations > or = 40 ng lipopolysaccharide per ml. The lipopolysaccharide stimulates proliferation of the B9 cell line in a dose-dependent manner both when measuring the proliferation by thymidine incorporation and when using the MTT assay. However the LPS dose-response curve is different compared to the dose-response curve for IL-6. A sample containing 100 ng LPS/ml but no IL-6 would be estimated erroneously to contain 12 pg IL-6. The interference of lipopolysaccharide is totally abolished by the addition of polymyxin B to the samples but the addition has no effect on the IL-6 induced proliferation.
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PMID:Lipopolysaccharide in concentrations above 40 ng/ml stimulates proliferation of the IL-6-dependent B9 cell line. 771 31

We studied the plasma levels of tumor necrosis factor-alpha (TNF-alpha) interleukin-6 (IL-6) as well as the in vitro production of these cytokines by peripheral blood mononuclear cells, in 10 patients with amebic liver abscess (ALA) and seven healthy controls. TNF-alpha was measured using a bioassay with L929 fibroblasts; IL-6 was quantitated by the B9 cell line assay. In both assays, the number of viable cells was estimated by the conversion of MTT to formazan. TNF-alpha plasma levels were nondetectable (< 20 pg/mL) in ALA patients, as well as in the majority of healthy controls. The in vitro production of TNF induced by lipopolysaccharide was significantly decreased in ALA patients. Most ALA patients (8/10) had increased plasma levels of IL-6. Furthermore, the spontaneous production of IL-6 in vitro was significantly increased in ALA patients compared to controls. In the acute stage of the ALA, a negative relationship was found between the raised plasma levels of IL-6 and the in vitro diminished production of TNF-alpha. After recovery, ALA patients showed both normal plasma levels and in vitro production of TNF and IL-6. Our data corroborate previous reports regarding plasma levels of TNF in ALA, and suggest that E. histolytica induces the in vivo production of IL-6 through a TNF-independent pathway. The raised levels of IL-6 might in turn down-regulate the production of TNF in ALA patients.
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PMID:Plasma levels and in vitro production of tumor necrosis factor-alpha and interleukin-6 in patients with amebic liver abscess. 797 44

Responses and susceptibility of 14 human glioblastoma cell lines to human natural tumor necrosis factor-alpha (TNF) were studied in vitro. Susceptibility of glioblastoma cells to TNF varied in experimental conditions applied. Most of glioblastoma cell lines were resistant to cytotoxic activity of TNF in a MTT assay at concentrations below 16 U/ml for 72 h exposure. However, TNF at higher dose, in prolonged exposure and against low density of target cells was antiproliferative for certain glioblastoma cultures. TNF exposure at 10 U/ml for 48 h suppressed DNA synthesis in 9 of 14 glioblastoma cultures, but increased in 3 cultures. In addition, colony forming assay showed anti-clonogenic activity of TNF in 5 of 6 glioblastoma cell lines tested. In spite of their low susceptibility to TNF, glioblastoma cells well responded to TNF stimulation at low dose (10 U/ml) for a short period in the absence of cell damage. Productions of Interleukin-6 (IL-6), IL-8-like activity, granulocyte-macrophage colony stimulating factor (GM-CSF), prostaglandin E2 (PGE2) and manganous superoxide dismutase (Mn-SOD) were enhanced or induced by the low-dose TNF stimulation. Mn-SOD, a protein protective against oxidative cell damage, was well induced in time- and dose-dependent manner, however did not correlate with TNF resistance. Whereas the levels of PGE2 in TNF-susceptible cell lines, H-4 and SF-188, were higher than those of other lines. In conclusion, most of glioblastoma cells are resistant to TNF cytotoxic effects, but highly responsive to TNF stimulation. Its effect on glioblastoma cells appears to modulate cell differentiation rather than to kill the cells.
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PMID:Responses of human glioblastoma cells to human natural tumor necrosis factor-alpha: susceptibility, mechanism of resistance and cytokine production studies. 836 Jul 7

The legal procedure for evaluating the toxicity of cosmetic, household, chemical and pharmaceutical products is still the irritancy Draize test on rabbits. Various irritation tests are currently being developed as alternatives to in vivo animal testing. Our in vitro model system is composed of 24 equivalent dermis (ED) comprising a chitosan-cross-linked collagen-glycosaminoglycan matrix populated by foreskin fibroblasts. In evaluating this system for irritancy testing, three different measures of toxicity were used: MTT (dimethylthiazol diphenyltetrazolium bromide) reduction, and lactate dehydrogenase and interleukin-6 release. The experiments described herein represent a preliminary evaluation to determine the usefulness and predictive value of our 24 ED kit as an alternative method for the prediction of human dermal reaction, versus three chemical products: cadmium chloride, lauryl sulfate, and benzalkonium chloride. Preliminary results suggest that the ED may be a useful in vitro model for the prediction of cutaneous and ocular toxicity and allow the development of a 24-skin-equivalent kit realized by seeding human normal keratinocytes onto the equivalent dermis.
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PMID:Pharmacotoxicological applications of an equivalent dermis: three measurements of cytotoxicity. 856 46

Inclusion complexes of gamma-cyclodextrin and octamethylcyclotetrasiloxane (D4), decamethyltetrasiloxane (M10TS), and 1,3,5,7-tetramethyltetravinylcyclotetra - siloxane (TMTV-D4) were prepared to compare the cytotoxic effects of siloxanes in vitro. In these preparations, the hydrophobic siloxanes are surrounded by a hydrophilic shell of eight circularly linked D-glucose molecules (gamma-cyclodextrin), and upon contact with plasma membranes the siloxane molecule can intercalate into the lipid bilayer of the cell membrane. XRPC24, 2-11 plasmacytoma, CH12.LX lymphoma and P388D1 macrophage-like cells were used as indicator cells in toxicity assays. Using an MTT tetrazolium reduction to formazan test, a colorimetric method to determine the number of viable cells, the 50% minimal lethal doses (CD50) for the siloxane compounds were found to range from 30 to 50 microM. Sublethal doses (e.g., 15 microM and lower) resulted in the loss of lactate dehydrogenase (LDH) and glutathione (GSH) from the cytosolic compartment of the target cells and thus indicated cytotoxicity. Treatment of macrophages with siloxanes resulted in a higher production of interleukin-6 (IL-6) than was exhibited by untreated macrophages. The B9 cell bioassay of these treated cells showed as much as a 10 fold higher production (500 U/ml) of IL-6 than did the untreated cells. The degree of increase was dependent on the compound and concentration used. The results of this study show that low molecular weight siloxanes produce lethal effects on B-lymphocyte derived target cells in vitro and permeabilize the plasma membranes at lower sublethal concentrations.
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PMID:Cytotoxicity and membrane damage in vitro by inclusion complexes between gamma-cyclodextrin and siloxanes. 856 93

Internal deletion K128-Q175 of the human interleukin-6 (hIL-6) has been generated at the cDNA level. With pBV220 as expressing vector, the recombinant pBV*-DIL-6 encoding the deletion mutant (12 kD) of hIL-6 has been constructed. The resulted recombinant plasmids were then used to transform E. coli strain HB101, and the expression in the PLPR promoter system, which is temperature-regulatable, was achieved. After purification and renaturation, the biological activity of the expressed product, designated as DM120, was measured by MTT method in an IL-6-dependent cell line 7TD1. The results show that the amino acid residues of IL-6 128 to 175 are crucial for IL-6 activity. Receptor binding assay in vitro indicates that the entire region is not involved in forming the receptor binding surface.
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PMID:Residues K128-Q175 of human interleukin-6 are essential for its biological activity. 928 73

The aim of the study was to investigate whether lactoferrin can improve the immune competence of cells from patients with systemic inflammatory response syndrome (SIRS). We studied the effect of lactoferrin (LF) on the proliferative response of peripheral blood mononuclear cells (PBMC) to lipopolisaccharide (LPS) in vitro and its influence on production of 2 proinflammatory cytokines: interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha). Three groups of patients: septic survivors, septic nonsurvivors and multiple trauma patients, were investigated. Blood samples were taken upon admission to intensive care unit and after 2, 3 and 5 days. The proliferative response of PBMC in vitro was tested using 3-day culture with LPS. Cell proliferation/death was measured using MTT colorimetric method. The spontaneous and LPS-induced activity of TNF-alpha and IL-6 were measured with bioassays using indicator cell lines WEHI-164.13 and 7TD1, respectively. We demonstrated that LF inhibited the proliferative response, both spontaneous and LPS-induced, in all groups of patients. Lactoferrin alone was a good inducer of IL-6 and TNF-alpha production by monoclear cells in vitro. Addition of LF to the cultures of LPS-activated mononuclear cells stimulated IL-6 production, most markedly in the group of septic survivor patients (mean 1479, 1452, 1728, 1980 pg/ml on day 1, 2, 3 and 6 respectively). Lactoferrin also upregulated TNF-alpha production. That effect was very significant in the septic survivor patients (mean 7407, 6739, 7498 and 8509 pg/ml on day 1, 2, 3 and 5 respectively) and less pronounced in the group of trauma patients. We conclude that lactoferrin exhibited regulatory actions on the altered reactivity of PBMC from patients with sepsis and multiple injury. Lactoferrin is a good inducer of IL-6 and TNF-alpha production. However, in most cases of septic nonsurvivors LF could not abolish low reactivity of cells with regard to cytokine production.
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PMID:Lactoferrin effects on the in vitro immune response in critically ill patients. 970 49

The therapeutic antitumor effect of clarithromycin (CAM) was examined with the 13762NF mammary adenocarcinoma and F-344 rat system. When CAM treatment at a dosage of 2 mg/kg of body weight orally for 21 days was commenced after inoculation of the tumor, no significant decrease in death rate was observed, although the loss in body weight was less than that in the untreated group. When tumor-bearing (TB) rats were treated with CAM in combination with carboplatin or cyclophosphamide, a significant decrease in the death rate was obtained, although neither treatment alone proved to be effective. A beneficial effect was also observed when CAM treatment was combined with surgical treatment. CAM showed no direct cytotoxicity to this tumor in vitro according to the MTT (3-[4, 5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay. Spleen cells obtained from TB rats receiving CAM treatment showed a stronger tumor-neutralizing activity than those from rats which had not received CAM treatment (Winn assay). Enhanced induction of cytotoxic cells to allogeneic tumor was also observed in rats immunized with allogeneic tumor cells together with CAM treatment (51Cr release assay). The 13762NF tumor produces transforming growth factor-beta (TGF-beta), tumor necrosis factor alpha, and matrix metalloproteinase-9, and treatment of tumor cells with CAM in vitro for 24 h significantly inhibited the expression of the genes coding for these proteins (reverse transcription-PCR). Levels of expression of the TGF-beta and interleukin-6 genes of spleen cells obtained from CAM-treated TB rats were both significantly lower than those of spleen cells from CAM-untreated TB rats. This study suggests that CAM has biological response modifier activities resulting in a beneficial therapeutic antitumor effect and might be useful for the treatment of human cancers.
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PMID:Therapeutic effect of clarithromycin on a transplanted tumor in rats. 986 67

In order to investigate the interaction of preserved solid lipid nanoparticles (SLN) with murine peritoneal macrophages (Mpsi), cytotoxicity and proinflammatory effects of two different solid lipid nanoparticles (SLN) preparations consisting of either compritol (CO) or cetyl palmitate (CP) preserved with thiomersal were analyzed. Concentration-dependent cytotoxic effects were observed using the 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyl-tetrazolium bromide (MTT) assay. Secretion of interleukin-6 by Mpsi following incubation with CO and CP SLN did not differ from secretion by untreated cells; proinflammatory cytokines interleukin-12 and tumor-necrosis-factor-alpha as further indicators of immunomodulatory effects were not detectable. These findings paralleled our previous findings that unpreserved CO and CP SLN did not induce immunomodulatory effects but cytotoxicity at higher concentrations. There were no synergistic cytotoxic effects of preservative and SLN. Thus, preservation of SLN using thiomersal does not appear to cause increased cytotoxicity and immunomodulatory effects following incubation with Mpsi.
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PMID:Preserved solid lipid nanoparticles (SLN) at low concentrations do cause neither direct nor indirect cytotoxic effects in peritoneal macrophages. 1069 26

Conventional lactate (Lac)-buffered peritoneal dialysis (PD) solutions have turned out to be detrimental to human peritoneal cells, especially because of a low pH. In the present study, we focus on potential differences between Lac and bicarbonate (Bic) as a buffer when adjusted to a physiological pH. All test fluids were buffered with either 40 mmol/L of Lac or 34 mmol/L of Bic, sterile filtered, and adjusted to a pH of 7.4. Osmotic agents used were 1.36% glucose (Glu), 3.86% Glu, 1% amino acids (AA), and 7.5% Glu polymer (Glupoly). Human peritoneal mesothelial cells (HPMCs) were isolated from the omentum majus, grown to confluence, and incubated after the second passage for 15 minutes (37 degrees C and 5% carbon dioxide) with the test fluids. Cytotoxicity was controlled by measuring apoptotic and necrotic cells with cytofluorometry. Aerobic cell metabolism (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide [MTT] assay) and intracellular adenosine triphosphate (ATP) concentrations were measured to assess cell viability. Release of interleukin-6 (IL-6) from HPMCs was determined as a parameter of cellular host defense. No significant difference in apoptosis or necrosis rates was found between the solutions adjusted to normal pH. However, in the MTT assay, Bic solutions were superior to corresponding Lac pendants at an identical pH of 7.4 (P < 0.01). Intracellular ATP concentrations reflected a very similar pattern (P < 0.05). Glupoly in combination with Lac showed an impaired pattern with both the MTT and ATP assays. Regarding IL-1beta-stimulated IL-6 release, there was a small, but not significantly better, response for Bic. Differences in manifest cell cytotoxicity reflected by apoptosis and necrosis rates could not be detected comparing PD solutions buffered with Lac or Bic at a physiological pH. However, distinct parameters of cell metabolism were superior with Bic compared with Lac. Especially Glupoly was inferior in combination with Lac as a buffer.
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PMID:Peritoneal dialysis fluids with a physiologic pH based on either lactate or bicarbonate buffer-effects on human mesothelial cells. 1157 93


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