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)

Normal peritoneal macrophages from C3H/He mice could not lyse syngeneic MM46 tumor cells in co-operation with syngeneic antitumor antibody. Thus, normal macrophages could not effectively participate in the antibody-dependent macrophage-mediated tumor lysis in vitro. However, after activation in vivo by stimuli, such as lipopolysaccharide, BCG, or glycogen, macrophages could co-operate with antitumor antibody in cytolysis of target cells. In the cytolysis nonspecific activation of normal macrophages was an essential first step, followed by specific tumor lysis in the presence of an antitumor antibody (second step). Immune macrophages from resistant mice were apparently equal in functional state to activated macrophages. A two-step mechanism of tumor lysis in vitro in a syngeneic mammary tumor system is proposed.
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PMID:Two-step mechanism of macrophage-mediated tumor lysis in vitro. 79 28

Endogenous mouse mammary tumor virus (MMTV) proviral transcripts are up regulated during the normal course of B-lymphocyte differentiation. We report here that the regulatory mechanisms which lead to increased levels of MMTV transcripts in differentiating, lipopolysaccharide (LPS)-stimulated normal B cells and in the inducible B-cell lymphoma line CH12 are at least partially distinct from those controlling increases in immunoglobulin and J-chain gene expression. In studies designed to characterize the stimulatory pathways leading to MMTV expression in CH12 cells, we found that stimulation with either LPS or dexamethasone (Dex), a transcriptional activator of MMTV genes, induced not only MMTV expression but also differentiation to antibody secretion. Only Dex-induced and not LPS-induced MMTV expression and differentiation were inhibited by the glucocorticoid antagonist RU486, demonstrating that Dex and LPS stimulate B cells by distinct molecular pathways. Therefore, in B cells, MMTV expression can be regulated via either the conventional hormone receptor-dependent pathway or a hormone receptor-independent pathway. Furthermore, these results suggest that steroid stimulation of B cells can lead to alterations in the expression of other results suggest that steroid stimulation of B cells can lead to alterations in the expression of other steroid-responsive genes that can become involved in the process of B-cell differentiation.
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PMID:Lipopolysaccharide and dexamethasone induce mouse mammary tumor proviral gene expression and differentiation in B lymphocytes through distinct regulatory pathways. 216 35

Expression of mouse mammary tumor virus (MMTV) in the lactating mammary glands of uninfected mice varies between strains of mice in a manner largely independent of the proviral content. Previous linkage analysis in the mouse suggested that the Lps locus was associated with steady-state levels of MMTV RNA. The Lps locus mediates the mouse's response to the injection of lipopolysaccharide (LPS) in the responder mouse while mice with the deficient allele are incapable of responding. Injecting LPS-responder mice, C3HfB/HeN, and nonresponder mice, C3Hf/HeJ, with LPS resulted in a threefold increase in the level of MMTV RNA in responder mice but had no effect on nonresponders. The increased level was due to only one of the possible MMTV transcripts: the 1.7-kb transcript containing the open reading frame (orf) of the long terminal repeat (LTR). The level of MMTV-specific transcripts, then, is regulated by the Lps locus, a cellular gene which is not linked to any viral coding sequences and therefore must act in trans.
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PMID:Mouse mammary tumor virus gene expression regulated in trans by Lps locus. 299 65

The effects of dietary soybean oil (SBO) concentration (5 vs. 20% by weight) on mammary tumorigenesis, mitogen-induced blastogenesis, cell-mediated cytotoxicity and serum and lymphocyte fatty acid composition were studied in C3H/OUJ female mice. Weanling mice fed 20% SBO for 9 mo had a higher incidence (89 vs. 65%) and greater average size (2.9 vs. 1.9 g) of mammary tumor virus type S breast tumors than mice fed 5% SBO. The response of isolated splenocytes to the T-cell mitogens concanavalin A and phytohemagglutinin was 20-25% lower in mice fed 20% SBO than in mice fed 5% SBO for 20 wk. There was no effect of SBO concentration on the splenocyte response to lipopolysaccharide E55:B5, a B-cell mitogen, or to pokeweed mitogen, and B- and T-cell mitogen. Cell-mediated cytotoxicity to allogenic P815 tumor cells was 20% lower in mice fed 20% SBO than in mice fed 5% SBO for 12 wk. The lower cell-mediated immunity associated with 20% SBO was not due to changes in the fatty acid composition of the two major splenocyte membrane phospholipids, phosphatidylcholine and phosphatidylethanolamine. However, serum levels of linoleic acid were higher in mice fed 20% SBO. Raising dietary SBO from 5 to 20% by weight was associated with increased mammary tumorigenesis, reduced T-cell blastogenesis and lower cell-mediated cytotoxicity.
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PMID:Lymphocyte activation, cell-mediated cytotoxicity and their relationship to dietary fat-enhanced mammary tumorigenesis in C3H/OUJ mice. 358 50

Sensitivity to macrophage-mediated cytostasis was determined with 4 tumor cell lines derived from a single, spontaneously arising mouse mammary tumor. Cytostasis was measured in a 48-hour [3H]thymidine-incorporation assay with the use of maleic vinyl ether (pyran) fraction 2 (MVE-2)-elicited peritoneal macrophages as effector cells. Metastatic tumor lines 66 and 410.4 were less sensitive than nonmetastatic lines 67 and 168. Pretreatment of tumor cells with indomethacin for 24 hours before assay increased the cytostatic sensitivity of the metastatic tumor lines but did not affect that of the nonmetastatic tumor lines. Addition of 100 ng lipopolysaccharide (LPS)/ml to the assay mixture of MVE-2-primed macrophages and tumor cells or pretreatment of macrophages with LPS markedly lessened the differences in cytostatic sensitivity among the metastatic and nonmetastatic lines. Pretreatment of tumor cells with indomethacin plus addition of LPS during the effector phase of the assay completely abrogated differences in sensitivity. These results suggest that differences in sensitivity of metastatic versus nonmetastatic tumor cells to macrophage cytostasis are due to both tumor cell (prostaglandin) and effector cell (activation state) factors.
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PMID:Differential sensitivity of metastatic versus nonmetastatic mammary tumor cells to macrophage-mediated cytostasis. 386 7

The mouse mammary tumor MT 296 was used in a further series of experiments on the implantation of tumor, plated out in vivo, from suspensions of individual cells. Lipopolysaccharide from S. typhosa was shown to exert an adjuvator influence. But this adjuvator, an endotoxin, had no direct effect on the suspended tumor cells, unlike the liver preparations previously reported. Lipopolysaccharide from S. typhosa was shown to act on the host. It made the host's connective tissue expanses more susceptible to successful implantation by the tumor cells. It did this only if present at the time these connective tissue expanses were split. The increased susceptibility, caused by splitting the connective tissue expanses in the presence of lipopolysaccharide, declined quickly after 24 hr. The structural changes wrought upon the connective tissues by splitting them in the presence of lipopolysaccharide are described. They show kinship to a Schwartzman reaction of the local type. Their possible role in the adjuvator effect on the plating of single cell suspensions of this tumor is discussed.
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PMID:Endotoxin as adjuvator to the transplantation of a mouse mammary tumor. 568 80

Inbred RIII mice, known to be infected neonatally with murine mammary tumor virus so that females develop mammary adenocarcinoma by 12-15 months of age, were examined with regard to antisheep red blood cell antibody responses at the cellular level. Female mice, 3-11 months old, compared to male mice of the same ages had consistent and significant depression of the antibody response of their splenocytes. Furthermore, female mice with adenocarcinoma showed an even greater depression of the antibody response. Spleen sizes were consistently increased in females as compared to those of male mice throughout the first year of life. The blastogenic responsiveness of the splenocytes to the B-cell mitogen Escherichia coli lipopolysaccharide and the T-cell mitogen phytohemagglutinin-P was not significantly different between male and female mice during the same periods, although the responses of the older tumor-bearing female mice to phytohemagglutinin-P were lower than those of non-tumor-bearing female mice. A complex relationship between age, sex, and immune responsiveness was evident in these mammary tumor virus-infected mice, which made it difficult to attribute a specific immune event to emergence of the mammary adenocarcinomas in the female as compared to male mice.
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PMID:Age- and sex-related differences in antibody formation and blastogenic responsiveness of splenocytes from RIII mice developing virus-induced mammary adenocarcinoma. 627 37

ONO-4007 is a novel synthetic analog of lipid A subunit and has been shown to exert antitumor activities on various experimental tumors with less toxicity than lipopolysaccharide. It remains unclear, however, what biological activities of this compound are relevant to its antitumor effects. We therefore investigated the activation of macrophages by ONO-4007 in vitro and in vivo and its implication in antitumor effects, using mouse MM46 mammary tumor as an experimental model. Intravenous injection of ONO-4007 produced significant therapeutic effects on this solid tumor. ONO-4007 could stimulate glycogen-elicited peritoneal macrophages in vitro, not only to produce tumor necrosis factor (TNF), but also to exert cytocidal activities against MM46 cells in vitro. Substantial TNF production was induced in tumor tissue by i. v. injection of ONO-4007, and its successive administration to tumor-bearing mice gave tumor-infiltrating macrophages a prominent in vitro tumoricidal activity and primed them for in vitro TNF secretion. These results suggest that activation of tumor-infiltrating macrophages to a direct tumoricidal state as well as to TNF secretion in tumor tissues may be at least some of the antitumor effects of this novel lipid A analog.
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PMID:Activation of tumor-infiltrating macrophages by a synthetic lipid A analog (ONO-4007) and its implication in antitumor effects. 816 10

Nitric oxide (NO) is a major effector molecule in the destruction of tumor cells by activated macrophages. However, in many cases, developing neoplasms appear to be capable of impairing steps in the complex process leading to NO production as a means of avoiding immune destruction. After activation with lipopolysaccharide (LPS), peritoneal-elicited macrophages (PEM) from mice bearing mammary tumors display alterations in their ability to lyse tumor cells due to reduced production of NO. In contrast, when these same cells are stimulated with LPS in combination with interferon gamma (IFN-gamma), they are able to produce NO and lyse targets at normal levels. Since tumor-associated macrophages are intimately associated with the cells of the developing tumor, their ability to produce NO and lyse tumor targets is likely to be more relevant to controlling tumor growth. This population of macrophages exhibited a more profound inability to produce NO and lyse targets and, unlike the PEM, was not able to upregulate these functions even when treated with combinations of LPS and IFN-gamma. Northern and Western blots revealed that inducible nitric oxide synthase (iNOS) mRNA and protein levels correlated directly with the ability of each macrophage population to produce NO, and the levels of these macromolecules were altered sufficiently in tumor bearers' macrophages to account for the diminished NO production described. These results indicate that a spatial gradient of suppression of macrophage cytolytic activity and iNOS expression exists in mammary tumor-bearing mice, whereby macrophages from within the tumor exhibit a more pronounced suppression than the more distally located PEM. This suppression may be due to proximity of the macrophages to the developing tumor, macrophage maturational state, or both.
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PMID:The altered tumoricidal capacity of macrophages isolated from tumor-bearing mice is related to reduce expression of the inducible nitric oxide synthase gene. 866 90

We studied the effects of conjugated linoleic acid (CLA) on lymphocyte function and growth of a transplantable murine mammary tumor. In experiment 1, eight-wk-old female Balb/c mice (n = 8/group) were fed 0.1%, 0.3% or 0.9% CLA for 3 or 6 wk. Lymphocyte proliferation, interleukin-2 production and lymphocyte cytotoxicity were assessed using splenic lymphocytes. Plasma CLA concentrations increased in a dose-dependent manner with CLA feeding. Lymphocyte proliferation in mice fed 0.3% and 0.9% CLA was enhanced in phytohemagglutinin-induced but not in concanavalin A- or lipopolysaccharide-stimulated cultures. Production of IL-2 also was stimulated by CLA. In contrast, CLA had no effect on lymphocyte cytotoxicity. In experiment 2, mice (n = 20/treatment) were fed the same diets for 2 wk before being infused with 1 x 10(6) WAZ-2T metastatic mammary tumor cells into the right inguinal mammary gland. Tumor volume and latency were recorded for 45 d. Dietary CLA did not affect mammary tumor growth. Tumor latency, tumor incidence and tumor lipid peroxidation activity also were unaffected by CLA. Body weight and feed intake were similar among treatments. Therefore, dietary CLA modulated certain aspects of the immune defense but had no obvious effect on the growth of an established, aggressive mammary tumor.
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PMID:Effects of dietary conjugated linoleic acid on lymphocyte function and growth of mammary tumors in mice. 913 39


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