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)

The fusion of thioglycollate-elicited peritoneal macrophages from lipopolysaccharide (LPS) non-responsive C3H/HeJ mice to an HPRT-negative variant of the murine macrophage cell line P388D1 has resulted in the derivation of a series of macrophage hybrids. Following exposure to LPS, these hybrids now produce the cytokine hepatocyte-stimulating factor (HSF) which induces the synthesis of the acute-phase reactant alpha 2-macroglobulin in primary rat hepatocyte cultures. The concentration of extracellular HSF was dependent upon both the duration and amount of LPS, with optimal HSF being detected after 72 hr incubation with 10 micrograms/ml of LPS. Parallel LPS-stimulated cultures treated with 10(-6)M dexamethasone did not secrete detectable amounts of HSF. Both the molecular weight (29,000 MW), and the fact that HSF activity was not inhibited by an antiserum directed against murine interleukin-1 alpha (IL-1 alpha), suggests that HSF and IL-1 are distinct cytokines. Therefore, macrophage hybrids have been derived which have acquired the LPS-responsive phenotype and which synthesize the cytokine HSF following LPS stimulation. This phenotype appears stable since similar results have been observed with these hybrids after in vitro culture for over 8 months.
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PMID:Restoration of the LPS responsive phenotype in C3H/HeJ macrophage hybrids: LPS regulation of hepatocyte-stimulating factor production. 332 5

Macrophages migrate through a fibrin-rich extracellular matrix in chronic inflammation, wound healing, and other pathophysiological processes. To investigate the factors that might influence the ability of mononuclear phagocytes to invade fibrin matrices, we cultured macrophage-like P388D1 cells as well as resident and thioglycollate-elicited mouse peritoneal macrophages on three-dimensional fibrin gels, and we examined the effect of agents known to stimulate a variety of macrophage functions, including the production of fibrinolytic enzymes. Cells grown on fibrin gels under control conditions, as well as cells treated with either bacterial lipopolysaccharide or concanavalin A, remained confined to the gel surface. In contrast, the tumor promoter 4 beta-phorbol 12-myristate 13-acetate (PMA) induced both P388D1 cells and peritoneal macrophages to invade the underlying fibrin matrix. The invasive behavior of PMA-treated P388D1 cells was not affected by protease inhibitors of various specificities. These results demonstrate that certain exogenous signals can profoundly modify the ability of macrophages to migrate through fibrin matrices.
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PMID:Phorbol ester stimulates macrophage invasion of fibrin matrices. 334 83

Tumor necrosis factor (TNF)-sensitive (LM) and -insensitive (P815) target cell lines were used to examine the role of TNF in both the activation and lytic phases of macrophage-mediated lysis. LM cells were lysed spontaneously by thioglycolate-elicited macrophages in an 18-h assay (media or activating agents added with targets) or 36-h assay (macrophages cultured with media or activating agents for 18 h, washed, and targets added for a subsequent 18 h). In contrast, P815 cells were lysed only in the 36-h assay by macrophages exposed to appropriate activation signals. Using antibody to murine TNF, it was shown that lysis of LM cells but not P815 cells was TNF mediated. The addition of lipopolysaccharide (LPS) to the 18-h assay resulted in augmented LM killing. This was probably due to the fact that LPS stimulates macrophages to produce TNF. Conversely, when macrophages were pretreated with LPS for 18 h, washed, and assessed for lytic activity during the subsequent 18 h, lysis of LM cells was reduced relative to the endogenous level. Although macrophage lysis of P815 was not mediated by TNF, the addition of TNF to macrophage activation cultures facilitated LPS triggering of cytolytic activity against P815. Similarly, the addition of TNF to the activation cultures partially prevented the LPS-induced reduction in macrophage-mediated LM cell lysis. Taken together, these data suggest that TNF may act as an autocrine signal during macrophage activation, in addition to being directly lytic to a select number of sensitive target cell lines.
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PMID:Role of tumor necrosis factor in macrophage activation and tumoricidal activity. 341 99

We studied various means of inducing avian phagocytes to migrate to the respiratory tract. No significant and consistent increases in the number of avian respiratory phagocytes (ARP) were elicited by intravenous inoculation with Escherichia coli lipopolysaccharide (LPS), Saccharomyces cerevisiae glucan (G), and Freund's incomplete adjuvant (FIA) in a water-in-oil-in-water emulsion; subcutaneous inoculation with the LPS-G-FIA homogenate; or aerosolized exposure to LPS-G-FIA, thioglycolate, and proteose-peptone. Intravenous inoculation with heat-killed Corynebacterium parvum resulted in a significant increase in the number of ARP by day 6 after inoculation; intratracheal inoculation of C. parvum effected a more rapid and higher level of phagocyte migration to the respiratory tract. Intratracheally administered E. coli induced significant migration of phagocytes to the respiratory system so that by 24 hours postinoculation, the group average number of ARP was about 50-100 times as high as the number in unstimulated control birds. None of the birds yielding high numbers of phagocytes from their respiratory tract had signs of respiratory disease.
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PMID:Cellular defense of the avian respiratory system. Influx of phagocytes: elicitation versus activation. 344 37

Protein synthetic patterns of murine peritoneal macrophages were analyzed by two-dimensional polyacrylamide gel electrophoresis (2D PAGE) of 35S methionine-labeled proteins. While the protein synthetic patterns exhibited by resident, inflammatory, and activated macrophages had numerous common features that distinguished them from the other normal non-macrophage cell types examined, unique proteins also characterized each macrophage population from the others. The accumulation by resident macrophages of proteins 23, 25, and 37 distinguished them from elicited cells, as did the former's more abundant synthesis of proteins 54 and 52. The protein synthetic patterns of inflammatory thioglycollate- and proteose peptone-elicited macrophages were strikingly similar, save for the former's greater levels of accumulation of proteins 14 and 28, and the latter's more pronounced expression of p23.5. Peritoneal macrophages elicited by treatment with heat-killed Propionibacterium acnes, the live, attenuated Mycobacterium bovis strain BCG, Listeria monocytogenes, and the protozoan flagellate Trypanosoma rhodesiense, all exhibited tumoricidal activity in 16-h or 72-h functional assays. They shared a common protein synthetic profile that differentiated them from the synthetic patterns characteristic of the non-tumoricidal resident and inflammatory macrophages. These tumoricidal macrophages were unique in synthesizing a protein(s) of approximate molecular weight 26,000 daltons. A time-course study employing P. acnes-activated peritoneal macrophages indicated that p26 accumulation decayed with tumoricidal capacity as a function of time in culture, although no direct correlation between lytic activity and p26 expression could be definitively established. Peritoneal macrophages elicited with proteose peptone were not directly tumoricidal but were rendered so upon in vitro treatment with nanogram amounts of bacterial lipopolysaccharide. The accumulation of low levels of p26 by the newly explanted proteose peptone-elicited macrophages suggests the possibility that this protein characterizes macrophage populations primed as well as triggered for tumoricidal activity.
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PMID:Differential protein synthesis by murine peritoneal macrophages elicited by various stimuli. 349 10

Two abortifacient proteins, alpha- and beta-momorcharin, have been purified from the seeds of the bitter melon (Momordica charantia). It was found that non-cytotoxic concentrations of these plant proteins can significantly inhibit the mitogenic responses of mouse splenocytes to concanavalin A, phytohaemagglutinin and lipopolysaccharide in a dose-dependent manner. In addition, the alloantigen-induced lymphoproliferation and the in vitro generation of a primary cytotoxic lymphocyte response were severely suppressed in the presence of these proteins. In contrast, the cytolytic activity of cytotoxic lymphocytes and natural killer cells was unimpaired by in vitro exposure to momorcharin. On the other hand, a clear decrease in the functional capacity of macrophages, such as the cytostatic and phagocytic activities, was observed under similar conditions. In vivo studies have shown that single injections of nontoxic microgram amounts of momorcharin into mice resulted in a significant depression of the delayed-type hypersensitivity response as well as the humoral antibody formation to sheep red blood cells. Similarly, the thioglycollate-induced in vivo migration of macrophages was also suppressed. Interestingly, the in vivo activation of natural killer cells was not appreciably affected. Our data suggests that the observed potent immunosuppressive effect of alpha- and beta-momorcharin is unlikely to be due to direct lymphocytotoxicity or due to a shift in the kinetic parameter of the immune response.
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PMID:The immunosuppressive activities of two abortifacient proteins isolated from the seeds of bitter melon (Momordica charantia). 349 34

Kinetics of peritoneal macrophage turnover during infection of mice with Salmonella enteritidis or following injection with thioglycollate broth or other peritoneal stimulants has been studied. Single intravenous injections of tritiated thymidine were given and the cells were examined by autoradiography. Maximum labelling of small adherent peritoneal macrophages occurred when 3H-thymidine was given 1 d after Salmonella and the cells were harvested 1 d later. Labelled cells decreased at later times despite maintenance of high numbers of macrophages in the exudates. Results from experiments in which labelled peritoneal cells were reinjected indicated that small, monocyte-enriched, labelled cells were not the major source of the large macrophages. Similar labelling at 2 d was observed using heat-killed Corynebacterium parvum or lipopolysaccharide (LPS) as ip stimulants. Following injection of thioglycollate broth, labelled peritoneal macrophages were only detectable if 3H-thymidine was given before the stimulant. These labelled cells remained longer in the peritoneal cavity. Labelling of and numbers of blood monocytes were consistent with the promotion of monocytopoiesis by Salmonella but not by thioglycollate. The response to thioglycollate but not Salmonella was dependent on the age of the mice. Animals injected with thioglycollate 1 d before Salmonella also had decreased resistance to bacteria and low numbers of labelled peritoneal macrophages. We propose that thioglycollate may recruit from a subset of preformed monocytes and temporarily block monocytopoiesis or macrophage bactericidal activity.
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PMID:Kinetics of macrophage recruitment and turnover in peritoneal inflammatory exudates induced by Salmonella or thioglycollate broth. 351 51

Goat mammary macrophage division in vivo was assessed by detection of mitotic figures, by autoradiographic measurement of the uptake of 3H thymidine, and by a 96-well proliferation assay. Autoradiography revealed that 3.74 +/- 0.77% of nonstimulated mammary macrophages were actively synthesizing DNA. Eight days of sterile inflammation, induced by lipopolysaccharide or thioglycollate, increased mammary macrophage division (10.9 +/- 2.1%). The division increased within 2 h after inducing inflammation with thioglycollate. After 1 day, the rate of division decreased, and another increase occurred 3-4 days later. The high rate of division was maintained for greater than 60 days after the induction of sterile inflammation. Division was further shown to occur by injecting 3H-thymidine directly into the mammary gland, harvesting the macrophages 1.5 h later, and determining incorporation by autoradiography. The results of all assays of division were in agreement, suggesting they reflected the same event. The dividing cells were nonspecific esterase-positive, adherent, motile, phagocytic, and had morphological characteristics of macrophages.
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PMID:Locally dividing macrophages in normal and inflamed mammary glands. 356 49

This work demonstrates the need for the continued presence of lipopolysaccharide (LPS) for tumor necrosis factor (TNF) production by thioglycollate-induced peritoneal macrophages. Removal of LPS at any time resulted in the abrupt cessation of further TNF production. The readdition of LPS resulted in further production of TNF but the yield was limited to the amount that would have been produced had the LPS not been removed.
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PMID:Requirement for the continual presence of lipopolysaccharide for production of tumor necrosis factor by thioglycollate-induced peritoneal murine macrophages. 372 20

Age related differences in macrophage responsiveness to adjuvants seen previously with thioglycollate induced cells were also found with resident macrophages. Thus, activation of phagocytosis by lipopolysaccharide, polyadenylic-polyuridylic acid complexes and muramyl dipeptides occurred when exposed to macrophages removed from young but not aging C58 and C3H/He mice. However, breeding status differences were observed in that aging virgin mice were unresponsive to these adjuvants, while aging breeder mice responded similarly to young virgin mice. Analysis of any changes in membrane phospholipids was carried out to determine their association with the age related and breeding status differences observed. Significant differences occurred in 32P labelling of phosphatidyl inositol between unstimulated macrophages from young and aging C58 mice. No differences were evident, however, after LPS stimulation. Analysis of macrophage plasma membranes from young and aging mice for cholesterol revealed significant age related differences in their ability to undergo increases in cholesterol content after LPS activation.
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PMID:Differential responses to adjuvants of macrophages from young virgin, aging virgin and aging breeder mice. 373 99


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