Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interleukin-6-(IL-6)-alpha dependent B-cell heterohybridomas were obtained by the fusion of X65.Ag8.653 cells with spleen cells from August rats immunized with lipopolysaccharide E. coli. One of these hybridomas (D6C8) was found to be most dependent on IL-6 for its surviving and growth. Human recombinant IL-1 beta and tumor necrosis factor-alpha could not induce the in vitro growth of this cell line. Presence of elevated level of IL-6 was demonstrated in the sera of patients with rheumatoid arthritis. A specific and sensitive detection of the IL-6 activity in test samples makes it possible to study the presence and role of IL-6 in various immunological disorders.
 ...
PMID:[The production and characteristics of an interleukin-6-dependent hybridoma]. 146 86

Both interleukin-1 (IL-1) and endotoxin (lipopolysaccharide, LPS) are potent activators of the hypothalamo-pituitary-adrenal (HPA) axis, and they also increase cerebral norepinephrine metabolism and tryptophan. Injections of cause macrophages to synthesize and release various cytokines, including IL-1 and tumor necrosis factor alpha (TNF alpha). The hypothesis that macrophage production of IL-1 mediates the HPA-activating effect of LPS was tested in mice using the IL-1-receptor antagonist protein (IRAP). Administration of IRAP largely prevented the effects of IL-1 alpha or IL-1 beta on the elevation of plasma corticosterone and the concomitant increase in hypothalamic norepinephrine metabolism, but failed to alter the responses to LPS. IRAP did not prevent the increases in brain tryptophan that occurred after treatment with IL-1 or LPS. Recombinant human TNF alpha, TNF beta, IL-6, and interferon-alpha injected intraperitoneally failed to activate the HPA axis, but mouse TNF alpha was effective by this route, and human TNF alpha, TNF beta, and IL-6 were effective intravenously. None of these cytokines was as potent as IL-1. Pretreatment with an antibody specific for mouse TNF alpha, either alone or in combination with IRAP, also failed to prevent the elevation of plasma corticosterone by LPS. Thus, either IL-1 and TNF alpha are not involved in the HPA and noradrenergic responses to LPS, or there are alternative (redundant) pathways by which LPS can activate the HPA axis.
 ...
PMID:The role of interleukin-1 and tumor necrosis factor alpha in the neurochemical and neuroendocrine responses to endotoxin. 147 14

The effect of interleukin 1 beta (IL-1 beta), interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF alpha) and lipopolysaccharide (LPS) on the expression of the C2 and C3 genes in human adherent monocytes was studied. Stimulation of monocytes with IFN-gamma increased both C2 and C3 mRNA. IL-1 beta also increased C2 mRNA level, whereas C3 gene expression was not enhanced. TNF alpha failed to increase either C2 or C3 mRNA. LPS increased C2 mRNA, but suppressed C3 gene expression. These results suggest that C2 and C3 production by monocytes is regulated by IL-1 beta and IFN-gamma in the local tissues.
 ...
PMID:Modulation of C2 and C3 gene expression of human peripheral blood monocytes by interleukin 1 beta, interferon gamma, tumor necrosis factor alpha and lipopolysaccharide. 147 81

We describe the development and application of a radioimmunoassay to detect circulating interleukin (IL)-1 beta concentrations in the rat. No IL-1 immunoreactivity above the detection limit of the assay (100 pg/ml) could be detected in plasma of control rats. In contrast, immunoreactive IL-1 was detected after intravenous administration of rat recombinant IL-1 beta (rrIL-1 beta) or bacterial lipopolysaccharide (LPS) to rats. The effect of LPS on plasma immunoreactive IL-1 concentrations was time and dose dependent. The immunoreactive IL-1 response to LPS was prevented by in vivo macrophage depletion induced by liposome-directed macrophage suicide technique. Gel filtration of plasma from LPS-treated rats revealed the presence of a high and a smaller molecular form of immunoreactive IL-1. The small molecular immunoreactive IL-1 peak coeluted with rrIL-1 beta and probably represents the 17-kDa form of IL-1 beta. In conclusion, our data support the hypothesis that IL-1 secreted by macrophages can act as a humoral signal molecule to induce the immunological, metabolic, and neuroendocrine changes in response to bacterial LPS.
 ...
PMID:Development and application of a radioimmunoassay to detect interleukin-1 in rat peripheral circulation. 147 82

The effects of 17 beta-estradiol (E2), progesterone (P) and testosterone (Te) on cell differentiation in the HL-60 promyelocytic leukemia cells after treatment with 1 alpha, 25-dihydroxyvitamin D3 [1,25-(OH)2D3] and those on interleukin-1 beta (IL-1 beta) production by HL-60 cells in response to lipopolysaccharide (LPS) were investigated. Neither E2 (10(-10) to 10(-7) M), P (10(-9) to 10(-6) M) nor Te (10(-10) to 10(-7) M) affected monocytic differentiation as assessed by reactivity with OKM14 monoclonal antibody and alpha-naphthyl acetate esterase activity. Pretreatment of HL-60 cells with 1,25-(OH)2D3 enhanced their ability to produce IL-1 beta in response to subsequent exposure to LPS, although 1,25-(OH)2D3 by itself did not induce IL-1 beta production by HL-60 cells. This priming effect of 1,25-(OH)2D3 was augmented by the addition of E2 and Te at physiologic concentrations, but not by that of P. E2, P and Te at physiologic concentrations enhanced IL-1 beta production by HL-60 cells that were pretreated with 1,25(OH)2D3 and stimulated by LPS. The increasing rate of IL-1 beta production by the addition of E2 and Te was higher when added with LPS than when added with 1,25-(OH)2D3. These findings suggest that enhancing effects of sex steroids in IL-1 beta production by monocyte/macrophage lineage cells.
 ...
PMID:Effects of sex steroids on cell differentiation and interleukin-1 beta production in the human promyelocytic leukemia cell line HL-60. 147 72

The production of interleukin 1 (IL-1) by lipopolysaccharide (LPS)-stimulated myelomonocytic cell lines ML-1, THP-1 and PL-21 was significantly enhanced by the addition of insulin, insulin-like growth factor (IGF)-I or IGF-II into the cell cultures. The IL-1 activity in the supernatants from cell cultures stimulated with LPS and insulin was completely neutralized by anti-IL-1 beta antibody. Anti-IL-1 alpha antibody had no inhibitory effect. Insulin itself did not stimulate IL-1 beta production directly, but increased it in the mitogen activated cells. However, insulin had no enhancing effect on the production of IL-1 alpha by human T cell lymphotropic virus-I (HTLV-I)-infected T cell lines or on IL-2 production by mitogen-stimulated leukemia T cell lines. Thus, insulin and its related cytokines are shown here as other molecules selectively modulating the production of IL-1 beta in myelomonocytic cell lines.
 ...
PMID:Selective enhancement of interleukin 1 beta production in myelomonocytic cell lines by insulin and its related cytokines. 148 10

Transforming growth factor beta (TGF-beta) and interleukin 1 (IL-1) are among the most potent osteotropic cytokines. The expression of mRNA for both TGF-beta and IL-1 beta was studied in human osteoblast-like cells in vitro. These cells constitutively expressed TGF-beta but not IL-1 beta mRNA. Treatment of the cells with the systemic hormones 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] (10(-8) M) and parathyroid hormone (10(-7) M) induced an increase in TGF-beta mRNA but failed to stimulate the production of IL-1-beta mRNA. Retinoic acid (10(-8) M) had no effect on either mRNA species. The cytokines IL-1 alpha (200 pg/ml), tumour necrosis factor alpha (TNF-alpha) (17 ng/ml) and bacterial lipopolysaccharide (LPS) (500 ng/ml) stimulated the production of IL-1 beta mRNA after 6-8 hours. This was followed by an increase in protein production after 24 hours. In contrast, the production of TGF-beta mRNA remained constant after treatment with these agents. Treatment of the cells with hydrocortisone (10(-8) M) resulted in the suppression of both TGF-beta and IL-1 beta mRNA. However, when the stimulating agent 1,25-(OH)2D3 was added in conjunction with hydrocortisone the mRNA expression of TGF-beta mRNA returned to 70% of the stimulated level. In contrast, the addition of the stimulatory agent IL-1 alpha to hydrocortisone-treated cells resulted in no increase in IL-1 beta mRNA. In-situ hybridization demonstrated both TGF-beta and IL-1 beta mRNA at the cellular level.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The transcriptional control of TGF-beta in human osteoblast-like cells is distinct from that of IL-1 beta. 149 52

Production of interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), interleukin 2 (IL-2), interferon gamma (IFN-gamma) and granulocyte-macrophage colony-stimulating factor (GM-CSF) after stimulation by lipopolysaccharide (LPS) and phytohemagglutinin (PHA) was studied in 1/10 diluted whole blood (WB) culture and in peripheral blood mononuclear cell (PBMC) culture. Cytokines IL-1 beta, TNF-alpha and IL-6 are preferentially stimulated by LPS whereas IL-2, IFN-gamma and GM-CSF are stimulated by PHA. Combination of 5 micrograms/ml PHA and 25 micrograms/ml LPS gave the most reliable production of the six cytokines studied. IL-1 beta, TNF-alpha and IL-6 represent a homogeneous group of early-produced cytokines positively correlated among themselves and with the number of monocytes in the culture (LeuM3). Furthermore, IL-1 beta was negatively correlated with the number of T8 lymphocytes. IL-2, IFN-gamma and GM-CSF represent a group of late-produced cytokines. Kinetics and production levels of IL-6 and GM-CSF are similar in WB and PBMC cultures. In contrast, production levels of TNF-alpha and IFN-gamma are higher in WB than in PBMC whereas production levels of IL-6 and IL-2 are lower in WB than in PBMC. Individual variation in responses to PHA + LPS was always higher in PBMC cultures than in WB cultures. The capacity of cytokine production in relation to the number of mononuclear cells is higher in WB, or in PBMC having the same mononuclear cell concentration as WB, than in conventional cultures of concentrated PBMC (10(6)/ml). Because it mimics the natural environment, diluted WB culture may be the most appropriate milieu in which to study cytokine production in vitro.
 ...
PMID:Direct stimulation of cytokines (IL-1 beta, TNF-alpha, IL-6, IL-2, IFN-gamma and GM-CSF) in whole blood. I. Comparison with isolated PBMC stimulation. 149 59

Fever and chills occur frequently with amphotericin B (AB) administration, but the mechanism that causes these reactions has not been definitively established. A variety of proinflammatory cytokines, including interleukin-1 (IL-1) and tumor necrosis factor, have been shown to be important mediators of fever. In order to clarify the cellular and biochemical responses associated with AB-induced fever, the experiments described sought to (i) establish whether human mononuclear cells exposed to AB in vitro expressed IL-1 beta, (ii) evaluate whether clinically used premedications for fever prophylaxis in AB-treated patients were effective in down-regulating IL-1 beta expression in vitro, (iii) evaluate whether methylxanthine agents with immunomodulatory actions effected in vitro IL-1 beta expression, and (iv) define the dose and time dependency of the modulating effects. Peripheral blood mononuclear cells were isolated by density centrifugation and resuspended to 10(6) cells per ml in culture wells of Linbro plates. When cocultured for 2 h with human mononuclear cells, both Escherichia coli lipopolysaccharide and AB stimulated IL-1 beta expression in a dose-related fashion. AB-induced IL-1 beta expression was suppressed by hydrocortisone (HC), pentoxifylline, and an investigational theobromine, A81-3138, in a linear, dose-related manner. In contrast, indomethacin, meperidine, and diphenhydramine had no effect on IL-1 beta expression. Our in vitro data indicate that serum HC concentrations of greater than 1 to 2 micrograms/ml may be sufficient to modulate IL-1 beta expression. Pentoxifylline and A81-3138 may also be effective in modulating IL-1 beta expression by mononuclear cells at concentrations achievable in serum. These new agents may prove to be effective alternatives to HC or may be added with HC to suppress febrile reactions secondary to AB administration. Clinical studies with pentoxifylline as a premedication for AB seem warranted.
 ...
PMID:Pharmacologic modulation of interleukin-1 expression by amphotericin B-stimulated human mononuclear cells. 151 Apr 23

Previous findings have shown that lipopolysaccharide (LPS)-activated human monocytes express cytokines (CKs) on their membrane. Furthermore, those associated to membrane products such as tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 have been demonstrated to exert many biological activities. In this paper, evidence is provided that human polymorphonuclear cells (PMN) exhibited an increased phagocytic capacity following incubation with either lipid A (LA)-activated autologous monocytes or supernatants recovered from LA-stimulated mononuclear cell cultures. In order to investigate the possible role of monocyte membrane-associated TNF-alpha, IL-1 alpha and IL-1 beta in the modulation of PMN activity, in a separate series of experiments LA-activated monocytes or LA-activated supernatants were pretreated with anti-recombinant human (Rhu) TNF alpha, anti-Rhu IL-1 alpha and anti-Rhu IL-1 beta monoclonal antibodies (MoAbs), respectively. Such an approach gave rise to an abrogation of monocyte-mediated triggering effect on PMN functional capacity. Taken together, these data suggest that activated monocytes can upregulate PMN phagocytosis by a cell-to-cell contact mechanism, likely related to membrane-associated CKs.
 ...
PMID:Enhancement of polymorphonuclear cell phagocytosis by lipid A-activated monocytes via cell-to-cell contact. A possible role for membrane-associated cytokines. 151 25


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>