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)

Escherichia coli lipopolysaccharide (LPS)-induced nitrate biosynthesis was studied in LPS-sensitive C3H/He and LPS-resistant C3H/HeJ mice. Intraperitoneal injection of 15 micrograms of LPS led to a temporary 5- to 6-fold increase in blood nitrate concentration in the C3H/He strain. Levels of nitrate excreted in the urine were also increased. In contrast, no increase was observed in the C3H/HeJ strain with LPS injections up to 175 micrograms. Furthermore, thioglycolate-elicited peritoneal macrophages from C3H/He, but not from C3H/HeJ mice, produced nitrite (60%) and nitrate (40%) when cultured with LPS (10 micrograms/ml). T-lymphocyte addition/depletion experiments showed the presence of T cells enhanced this response. However, LPS did not cause nitrite or nitrate production in cultures of spleen lymphocytes from either strain. LPS-induced nitrate synthesis was also observed with nude mice and CBA/N mice, indicating that neither functional T lymphocytes nor LPS-responsive B lymphocytes were required for the response in vivo. This was consistent with the in vitro results showing macrophages alone were competent. Mycobacterium bovis infection of C3H/He and C3H/HeJ mice resulted in a large increase in nitrate production over the course of the infection for both strains, suggesting T-lymphocyte-mediated activation of macrophages as a potent stimulus for nitrate biosynthesis. The synthesis of nitrite is significant in that it can directly participate in the endogenous formation of nitrosamines and may also be involved in some aspect of the chemistry of cytotoxicity.
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PMID:Mammalian nitrate biosynthesis: mouse macrophages produce nitrite and nitrate in response to Escherichia coli lipopolysaccharide. 390 50

RAW 264.7 cells upon stimulation with lipopolysaccharide secrete a protein mediator(s) that suppresses lipoprotein lipase activity in differentiated 3T3-L1 cells. The mediator(s), which is absent from unstimulated culture supernatants, is nondialyzable and thermolabile. Preliminary characterization suggests that this mediator(s) may be the same as that previously found in medium from lipopolysaccharide-treated thioglycollate-elicited mouse peritoneal macrophage cultures.
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PMID:Lipopolysaccharide-treated RAW 264.7 cells produce a mediator that inhibits lipoprotein lipase in 3T3-L1 cells. 396 30

The susceptibility of cloned cell lines of the 13762NF rat mammary adenocarcinoma to macrophage-mediated cytolysis was investigated using both intra- and extratumoral macrophages. The percentage of Fc receptor-positive cells in tumors growing s.c. in syngeneic F344 rats ranged from 8 to 20%, but we could not demonstrate a significant correlation between the number of Fc receptor-positive cells within tumors and their spontaneous metastatic potentials. In macrophage-mediated cytolysis assays, cloned 13762NF cell lines of differing metastatic potential, established from tissue culture lines, fresh tumor explants, or short-term cultures (one passage in vitro), were used as targets. Effector cells were thioglycolate-elicited peritoneal macrophages (activated in vitro with bacterial lipopolysaccharide) or intratumoral macrophages (activated in vitro with lipopolysaccharide). When the effector cells were peritoneal macrophages, established cloned 13762NF cell lines showed little correlation in their susceptibility to macrophage-mediated cytolysis and metastatic potential, while this was not observed when fresh tumor explants were used. Highly metastatic MTLn3 cells were the least sensitive, less metastatic MTF7 and MTLn2 cells were more susceptible, and the low metastatic parental MTPa cells were the most sensitive in 72-h cytolysis assays. When the effector cells were intratumoral macrophages, all 13762NF cell lines showed less sensitivity in cytolysis assays than similar assays using thioglycolate-elicited peritoneal macrophages. With the exception of line MTLn2, short-term cultures (one passage in vitro) did not differ substantially in susceptibility to intratumoral macrophages compared to fresh explants. In this system, the sensitivity of 13762NF cells to macrophage-mediated cytolysis is a function of effector as well as target cell source.
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PMID:Heterogeneity in the sensitivities of the 13762NF rat mammary adenocarcinoma cell clones to cytolysis mediated by extra- and intratumoral macrophages. 397 11

The capacity of non-activated murine thioglycollate-elicited macrophages and bone marrow-derived macrophages to lyse primitive F9 teratocarcinoma cells lacking H-2 antigens was investigated. Both populations of non-activated macrophages killed F9 cells efficiently whereas they were not cytolytic against murine fibrosarcoma targets. In vitro activation by lipopolysaccharide induced the macrophages to lyse fibrosarcoma cells but did not significantly increase the level of cytolysis against F9. These results are consistent with the hypothesis that the absence of H-2 expression on target cells may serve as a signal for macrophage "foreign" recognition and cytolysis.
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PMID:Lysis of primitive teratocarcinoma cells by non-activated macrophages. 404 17

Tissue transglutaminase accumulates rapidly and to very high levels (1-2% of cellular protein) in mouse peritoneal macrophages cultured in mouse serum. The induction is due to accelerated synthesis of the enzyme (150-fold increase) that occurs within 90 min of exposure of the cells to a heat-labile constituent of serum or plasma. The induction is reversible and is not reproduced by known activators of macrophage function such as lipopolysaccharide, muramyl dipeptide, and tuftsin. In animals, elevated levels of tissue transglutaminase are also found in inflammatory macrophages elicited by thioglycolate broth.
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PMID:Induction of tissue transglutaminase in mouse peritoneal macrophages. 613 12

The course of infection with herpes simplex virus type 1 (HSV-1) in peritoneal macrophages, phytohemagglutinin (PHA-)stimulated (T-)lymphocytes and lipopolysaccharide (LPS-)stimulated (B-)lymphocytes of NMRI-mice was studied by means of electron microscopy. Non-stimulated as well as thioglycolate-stimulated macrophages were investigated; lymphocytes were derived both from HSV-1-sensitized and non-sensitized animals. The morphological characteristics of the abortive infection in macrophages and T-lymphocytes and of the productive infection in B-lymphocytes are described. No differences were observed between stimulated and non-stimulated cells or cells of sensitized and non-sensitized animals.
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PMID:Electron microscopic studies of herpes simplex virus type 1 infection of macrophages, T- and B-lymphocytes of mice. 625 May 15

The regulation by prostaglandin E2 (PGE2) of production of oxygen radicals by bacterial lipopolysaccharide-(LPS) activated macrophages was studied in vitro. A 48-hr incubation of murine thioglycollate-elicited macrophages with LPS (0.1 micrograms/ml) resulted in an enhanced ability of these cells to produce oxygen radicals when challenged with phorbol myristate acetate (PMA). Macrophages incubated for 48 hr without LPS did not produce measurable amounts of oxygen radicals when exposed to this triggering stimulus. Thus, PMA-triggered production of oxygen radicals was the result of macrophage activation by LPS. The PMA-triggered production of oxygen radicals by the LPS-activated macrophages was inhibited when PGE2 (10(-5) to 10(-9) M) was present during the incubation with LPS. Inhibition by PGE2 occurred during the early stages of macrophage activation, since the addition of PGE2 24 hr after LPS no longer inhibited the production of oxygen radicals by the macrophages. This inhibitory effect of PGE2 on the LPS-induced activation of macrophages could be reproduced by cyclic-adenosine-monophosphate (cAMP) agonists, such as isoproterenol and cholera toxin as well as by the cAMP analog dibutyryl-cAMP, suggesting a cAMP-mediated mechanism for the inhibitory effect of PGE2 on macrophage activation by LPS. Previous reports have implicated prostaglandins as mediators of destructive processes associated with chronic inflammation. Our findings suggest that PGE2 may, on the other hand, reduce tissue damage in a chronic inflammatory site by inhibiting the production of oxygen radicals by macrophages activated in the sera.
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PMID:Regulation by PGE2 of the production of oxygen intermediates by LPS-activated macrophages. 626 31

Salmonellae with differences only in the O-antigenic polysaccharide of their lipopolysaccharide were previously shown to differentially activate complement via the alternative pathway, causing them to be ingested at different rates by the mouse macrophage-like cell line J774. We now show that this mechanism could explain the different virulence of these strains in vivo. Mouse peritoneal macrophages (thioglycolate induced) ingest these salmonellae at rates that are inversely proportional to the known virulence of the organisms and virtually identical to the rates observed with J774. As with J774, complement is required for this differential uptake, since serum was required and heating (56 degrees C for 30 min) or zymosan treatment of the serum destroyed activity. The known receptor for nonreducing terminal mannose-, fucose-, N-acetylglucosamine, and glucose-containing glyco-proteins did not participate, since uptake was not inhibited by high concentrations of mannan. When clearance of bacteria from the bloodstream of mice was measured, the least virulent organism was cleared very much faster than the most virulent organism, in confirmation of earlier data. When complement in the mice was destroyed by pretreatment with cobra venom factor, the clearance of the least virulent strain was greatly reduced, whereas the very slow clearance of the most virulent strain was unaffected. These data strongly support the hypothesis that when bacteria have polysaccharide in lipopolysaccharide that activates complement efficiently, the bacteria will be phagocytosed, whereas if the polysaccharide activates complement poorly, the bacteria escape ingestion and may cause disease.
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PMID:Complement activation by polysaccharide of lipopolysaccharide: an important virulence determinant of salmonellae. 634 90

Lectin-like molecules on the surface of murine peritoneal exudate macrophages induced by thioglycolate or an anti-tumor streptococcal preparation, OK-432, were investigated and isolated. Furthermore, their sugar-binding specificities and their role in macrophage-mediated tumor cytotoxicity were examined. A neoglycoprotein, D-galactose (Gal)-bovine serum albumin, bound to these murine peritoneal macrophages. This binding of Gal-bovine serum albumin was inhibited by D-galactose, and by complex-type oligosaccharides (unit B) and high mannose-type oligosaccharides (unit A) prepared from porcine thyroglobulin. When thioglycolate-elicited macrophages were activated by lipopolysaccharide and/or the culture supernatant of concanavalin A-activated mouse spleen cells, they became tumoricidal and the number of the lectin-like molecules on the macrophage surface was found to increase. Since the binding and cytotoxic activities of these tumoricidal macrophages toward tumor cells were partially inhibited by D-galactose, the D-galactose-binding lectin-like molecules on the surface of tumoricidal macrophages might play an important role in macrophage-mediated cytotoxicity. These lectin-like molecules were then isolated from solubilized murine peritoneal exudate cells labeled with pyridoxal 5'-phosphate and sodium [3H]borohydride by affinity chromatography on columns of asialo unit B oligosaccharide-Sepharose 4B and/or beta-D-galactose-Bio-Gel P-100. The proteins bound to the asialo unit B oligosaccharide-Sepharose 4B column and eluted specifically were found to have approximate molecular weights of 79 000 and 18 000, and the protein bound to and eluted from the beta-D-galactose-Bio-Gel P-100 column had an approximate molecular weight of 77 000. These isolated proteins bound to the surface of glutaraldehyde-fixed tumor cells, and their binding was inhibited by D-galactose and also by D-mannose. Since most of the 77 kDa protein bound to the asialo unit B oligosaccharide-Sepharose 4B, this protein was assumed to be identical with the 79 kDa protein. These results suggest that the lectin-like molecules on murine macrophages have wide specificity and that one lectin-like molecule can bind both D-galactose and D-mannose.
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PMID:Lectin-like molecules on the murine macrophage cell surface. 648 61

Peritoneal macrophages were obtained from DBA/2 mice that were untreated or after the injection of bacillus Calmette-Guerin (BCG), thioglycollate broth, proteose-peptone broth, or gamma-irradiated P-815 tumor cells. These macrophages were "activated" to become cytotoxic for a fibroblast cell line (L 929) by the addition of lymphokines (LKs), lipopolysaccharide (LPS), or fibroblast interferon (IFN-beta), and the expression of I region-associated antigens (Ia-Ad) on the macrophages was examined both before and after activation. Thioglycollate-elicited macrophages became Ia-A+ when activated by LKs, but they remained Ia-A- when activated by LPS or IFN-beta. Resident macrophages and proteose-peptone-elicited macrophages remained Ia-A- when activated with LKs. Macrophages from BCG-infected mice were both Ia-A+ and cytotoxic for tumor cells without further treatment. In contrast, macrophages from mice injected with gamma-irradiated P-815 mastocytoma cells were Ia-A+ but not cytotoxic, and these macrophages could not be made cytotoxic by incubation with LKs. The cultured macrophage-like cell lines P388D1 and WEHI-3 became Ia-A+ after incubation with LKs, and this treatment amplified the cytotoxicity of both cell lines. We conclude that a number of factors are important in determining whether Ia-A expression accompanies macrophage activation and that Ia-A is irrelevant as a surface marker for macrophage activation.
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PMID:Macrophage activation: dissociation of cytotoxic activity from Ia-A antigen expression. 657 60


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