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

We have studied the ability of purified B lymphocytes to generate cytotoxic T lymphocytes in autologous mixed leukocyte cultures (MLC). Cytotoxic lymphocytes were produced but only autologous mononuclear cells stimulated by lipopolysaccharide (LPS) were susceptible target cells. Unstimulated mononuclear cells and purified B cells were not susceptible to killing by cytotoxic cells generated in the autologous MLC. This suggests that the target antigen may be expressed on stimulated or dividing B lymphocytes in a way that renders the cells more susceptible to cytolysis. Autologously stimulated cytotoxic effector cells were found to exhibit specificity. Cy totoxicity for autologous LPS-stimulated target cells occurred but not for an allogeneic, B cell, histiocytic lymphoma cell line. It is postulated that cytotoxic T cells generated in the autologous MLC may play a role in immune surveillance or in regulation of the immune system.
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PMID:Generation of cytotoxic lymphocytes in the autologous mixed lymphocyte culture. 15 88

Long-term syngeneic radiation chimeras displayed a very low incidence of reticulum cell sarcoma as compared with control mice. Immune reactivity of these animals was studied in vivo by anti-dinitrophenyl antibody titer and affinity and in vitro by mitotic responsiveness to phytohemagglutinin, concanavalin A and lipopolysaccharide. Anti-body titer and affinity as well as the response to T lectins were found to be increased in chimeras. These results were attributed to increased function of mature T2 cells, which could explain the reduced incidence of reticulum cell sarcoma in chimeras.
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PMID:Immune responsiveness and incidence of reticulum cell sarcoma in long-term syngeneic radiation chimeras. 79 6

Treatment with 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and incubation with lipopolysaccharide (LPS) induces interleukin 1 beta (IL-1 beta) production in the histiocytic lymphoma cell line U937. Here we investigated the effect of treatment with both TPA and 1 alpha, 25-dihydroxyvitamin D3 (1,25(OH)2D3) on LPS-induced IL-1 beta production in U937 cells. To clarify the mechanism of IL-1 beta production, the possible role of polyamines in this process was examined. Combined treatment with TPA and 1,25(OH)2D3 for 72 h followed by incubation with LPS for 24 h caused synergistic induction of both IL-1 beta release and mRNA expression. On the other hand, TPA increased the numbers of vitamin D3 receptors, which may be one mechanism of this synergistic induction. Ornithine decarboxylase (ODC), a rate-limiting enzyme for polyamine biosynthesis, was also induced by these compounds biphasically: the first peak of ODC activity was observed at 4 h of the incubation with the two compounds and the second peak was at 4 h after the addition of LPS. To find whether these peaks were related to IL-1 beta production, DL-alpha-difluoromethylornithine (DFMO), a specific irreversible inhibitor of ODC, was added together with TPA and 1,25(OH)2D3. DFMO decreased the cellular levels of putrescine and spermidine and suppressed IL-1 beta release and IL-1 beta mRNA expression by 65%. Exogenous putrescine, but not spermidine, abrogated these kinds of inhibition. Similar results were obtained with DFMO and the polyamines during the differentiation of the cells up to the monocyte or macrophage stage. These results thus suggest that changes in either of these intracellular polyamines, especially putrescine, help to regulate the differentiation of U937 cells, resulting in partial control of the regulation of IL-1 beta production.
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PMID:Role of putrescine in interleukin 1 beta production in human histiocytic lymphoma cell line U937. 204 Jun 54

The monokine eosinophil cytotoxicity enhancing factor (ECEF) increases antibody-dependent cytotoxicity of eosinophils towards helminth larvae. A monokine biochemically indistinguishable from ECEF increases the release of leukotriene C4 and other arachidonic acid metabolites by eosinophils. We have developed monoclonal antibodies (mAb) to these monokines by immunizing mice with ECEF made by the U-937 histiocytic lymphoma cell line. mAb 81.10.C9 (IgG2b) and 9A6G (IgG1) inhibit the effect of the monokine on release of AA products. Both mAb bind ECEF, which appears after affinity chromatography purification as a major 13-14-kDa and a minor 62-kDa component (13-14 kDa and 52 kDa after reduction) in silver-stained gels. An additional component of 30 kDa is detectable after radioiodination of the immunopurified material. The specificity of both mAb was studied in several ways. In immunoprecipitation, both recognize the 13-14-kDa and the 30-kDa components, while the 62-(52)-kDa protein is not significantly precipitated. Both mAb react in enzyme-linked immunosorbent assay with products secreted by peripheral blood mononuclear cells and monocytes, as well as with those secreted by phorbol 12-myristate 13-acetate and lipopolysaccharide-stimulated U-937 cells and with the immunopurified proteins. These were separated in sodium dodecyl sulfate-polyacrylamide gel electrophoresis, electroeluted and assayed for ECEF activity. Activity was associated with the 13-14-kDa and the 30-kDa fractions, as seen by increased eosinophil antibody-dependent adherence to schistosomula and cytotoxicity. Granulocyte-monocyte-colony-stimulating factor and interleukin 1, but not tumor necrosis factor, could be detected in crude U-937 supernatants. However, active immunopurified ECEF has no activity in assays for granulocyte-monocyte-colony-stimulating factor, interleukin 1 or tumor necrosis factor. Immunocytochemical localization of ECEF employing the mAb shows strong surface staining of viable monocytes and U-937 cells, suggesting that ECEF is associated to the cell surface. These properties distinguish ECEF from other monokines previously reported to activate eosinophils.
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PMID:Eosinophil cytotoxicity enhancing factor: purification, characterization and immunocytochemical localization on the monocyte surface. 219 4

An epidemic of a malignant neoplasm occurs in northern pike, Esox lucius L., from the Aland Islands of Finland. The neoplasm is morphologically similar to other pike hemic tumors reported in other areas of the world. Pike normal tissues showed evolutionary conservation with the mammalian intermediate filament proteins cytokeratin, desmin, vimentin, neurofilament protein, and glial fibrillary acidic protein; tumor cells are positive for vimentin, suggesting that the neoplasm is of mesenchymal origin. Hemic tissue mononuclear cells undergo polyclonal stimulation by the known mammalian T- and B-lymphocyte mitogens phytohemagglutinin P, concanavalin A, tuberculin-purified protein derivative, and lipopolysaccharide W; pike tumor cells are nonreactive. Pike normal hemic tissue mononuclear cells are variously positive for surface and cytoplasmic immunoglobulins, using rabbit anti-pike immunoglobulin M and cross-reactive mouse anti-carp immunoglobulin M antibodies; tumor cells, however, are not positive. The tumor cells were also diffusely stained with sodium fluoride-sensitive nonspecific esterase. The foregoing suggest that the neoplasm is not of B-lymphocytic or plasmacytic derivation, while the T-lymphocytic as opposed to monocytic derivation cannot be excluded on the basis of marker studies. The ultrastructural studies, however, suggest a neoplasm of histiomonocytic derivation, while the absence of sinusoidal infiltration of tumor cells to head kidney, spleen, liver, or peripheral blood suggests that it is a piscine analogue of human true histiocytic lymphoma. Population dynamics studies indicate that the neoplasm affects primarily sexually mature males 5 to 6 yr of age, but does not at present appear to be a major factor affecting Aland pike populations.
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PMID:Immunological and ultrastructural characterization of true histiocytic lymphoma in the northern pike, Esox lucius L. 220 40

Recently, we have characterized a lymphocyte blastogenesis inhibitory factor (LBIF) which was purified from the culture supernatant of a human histiocytic lymphoma U-937 (Sugimura, K. et al., Eur. J. Immunol. 1989. 19: 1357). In this study, we investigated the effect of LBIF on the antibody production of autoimmune MRL mice in vitro. We demonstrated here that (a) LBIF inhibited the IgM, IgG and IgA antibody responses of lipopolysaccharide (LPS)-stimulated spleen cells of normal BALB/c mice, (b) in the case of old autoimmune MRL/Mp-lpr/lpr (MRL/l) and MRL/Mp-(+)/+ mice, however, LBIF inhibited IgM and IgA but not IgG responses of LPS-stimulated spleen cells, (c) the antibody production of all IgG subclasses, IgG3, IgG1, IgG2b and IgG2a, was not sensitive to LBIF inhibitory activity in these autoimmune mice, (d) in young MRL mice (3-5-week-old MRL/l), which were phenotypically normal, LPS-induced antibody production of all isotypes (IgM, IgG and IgA) was strongly inhibited by LBIF as shown in normal BALB/c mice and (e) in the case of 7-week-old MRL/l the insensitivity to LBIF was concomitant with the appearance of gamma + B lymphocytes. Thus, by employing LBIF as a probe, this study showed a correlation between the pathogenesis of MRL autoimmune disease and the lack of LBIF sensitivity of hyperactive B lymphocytes and suggested that the intrinsic abnormality of autoimmune MRL B lymphocytes might be confined to gamma- but not mu- or alpha-committed B cells.
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PMID:Abnormal behavior of gamma-committed B lymphocytes probed by a lymphocyte blastogenesis inhibitory factor in autoimmune MRL mice. 220 96

Neuroendocrine mechanisms are involved in modulation of the immune system, but the mode of action of the complex interplay between hormones and the immune system is only partially understood. This study examines the role of cortisol in monocyte differentiation and function, with regard to interleukin-1 beta (IL-1 beta) expression. The differentiation of the human histiocytic lymphoma cell line U 937 into macrophage-like cells by phorbol ester [phorbol myristate acetate (PMA)] is inhibited by cortisol. Some cells remain in suspension and continue to divide; others stop proliferation, but do not undergo full morphological differentiation. When cells are washed after 3 days to remove PMA and cortisol, all cells stop dividing and become fully differentiated. The PMA, therefore, commits the cells to differentiate even after its removal, while cortisol is only suppressive when present. Differentiated cells are shown to produce IL-1 beta mRNA when stimulated with lipopolysaccharide. This effect is inhibited by cortisol in a dose-dependent manner. After removal of cortisol, the least differentiated cells that remained in suspension were found to be overproducers of IL-1 beta mRNA after stimulation with lipopolysaccharide. This suggests that PMA induces a buildup of transcription-activating factors that were suppressed in the presence of cortisol. We conclude that the adrenal glucocorticoids that are elevated in acute stress conditions or major depression attenuate the differentiation and function of monocytes.
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PMID:Inhibition of macrophage differentiation and function by cortisol. 236 81

A stable human macrophage hybridoma was established by somatic cell fusion between human peripheral blood monocyte-derived macrophages and an 8-azaguanine resistant clone of a human histiocytic lymphoma cell line U-937 (clone U-937-F9). The hybrid cell line (F9P) exhibited typical macrophage-like morphology and had 30 more chromosomes than U-937-F9 cells. Its macrophage characteristics were confirmed by the manifestation of intracellular nonspecific esterase, the detection of Mo-2 and LEU-M3 antigens on the cell surface, and the demonstration of phagocytic activity. Furthermore, when stimulated with lipopolysaccharide (LPS), this cell line could secrete a considerable amount of a cytotoxic factor (CTF). Distinct from the hybrid cell line, the parental U-937-F9 cells expressed neither Mo-2 nor LEU-M3 antigens on the cell surface, did not show phagocytic activity, and their culture supernatants did not show cytotoxic activity even after LPS stimulation. The activity of CTF in the culture supernatant of the LPS-stimulated hybrid cells could not be neutralized with anti-tumor necrosis factor, anti-interleukin-1, or anti-lymphotoxin antibodies. The CTF had a relative molecular mass of 45-60 x 10(3) daltons as determined by gel filtration on a column of Superose 12, and an isoelectric point of 5.1. The cytotoxic activity was also induced when the hybrid cells were stimulated with the concentrated supernatants of a human T-cell hybridoma containing macrophage activating factor for cytotoxicity or with LP3 tumor cells which were used as target cells.
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PMID:A human macrophage hybridoma producing a cytotoxic factor distinct from TNF, LT, and IL-1. 325 90

Although the murine reticulum cell sarcoma M5076 is highly malignant in vivo, in vitro it displays many of the functional characteristics of an activated macrophage, such as phagocytosis and tumor cytotoxicity. This study was designed to determine what effect macrophage-activating agents would have on the function and growth of M5076 cells. Exposure of M5076 tumor cells to substances that activate normal macrophages to the tumoricidal state rapidly and irreversibly induced cessation of cellular division. The treated tumor cells, however, retained the same characteristics as those of untreated M5076 cells in vitro with respect to viability and the activated macrophage functions of phagocytosis and tumor cytotoxicity. Even after a short exposure to lipopolysaccharide, the ability of M5076 cells, injected i.v. into syngeneic mice, to form tumor nodules was greatly reduced. These results indicate that a highly malignant tumor of macrophage origin, M5076, can be induced to cease cellular division while retaining the functional attributes of an activated macrophage. We speculate that the exposure of M5076 to macrophage-activating agents results in the induction of terminal differentiation of this tumor.
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PMID:Inhibition of cellular division of a murine macrophage tumor by macrophage-activating agents. 703 20

Epinecidin-1, an antimicrobial peptide documented in some fish, is an essential component of the innate immune response in fish, but little is known about its gene regulation. To better understand the molecular mechanism controlling transcription of the epinecidin-1 gene, we cloned and sequenced the genes and promoter regions of three epinecidin-1 peptides from the grouper (Epinephelus coioides). These genes have the potential to encode three putative epinecidin-1 peptides with either a short or a long 5'-untranslated region (UTR). These epinecidin-1 genes, numbered 124-1 (gene structure: 5 exons), 124-2 (gene structure: 5 exons), and 961 (gene structure: 4 exons), have 3' UTR sequences that dramatically differ by being located on different exons in clones 124 and 961. To address the roles of lipopolysaccharide (LPS) and poly(I):poly(C) in regulating epinecidin-1 expression, serial deletions were prepared in the promoter region of two clones that contained three genes. Different fragments of the epinecidin-1 5'-flanking region were transfected into U937 (human histiocytic lymphoma) and ZFL (zebrafish liver) cells and then treated with 0, 1, 10, and 100 mug/mL LPS or poly(I):poly(C). The results showed that after treatment with 10 mug/mL LPS, high promoter activity was observed in the 0.6-kb promoter fragment (of clone 961). Promoter deletions showed that hepatocyte nuclear factor (HNF)-1 was required for a maximal response of epinecidin-1 961 promoter activity after LPS treatment in ZFL cells. Morphological studies of transgenic zebrafish indicated that the 2-kb epinecidin-1 124-1 promoter-driven GFP transcripts appeared in the eye and skin as confirmed by immunohistochemical staining. These results indicate that the 2-kb epinecidin-1 124-1 promoter is active in a tissue-specific manner.
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PMID:Organization and promoter analysis of the grouper (Epinephelus coioides) epinecidin-1 gene. 1851 59


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