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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to determine whether the bacterial bone resorbing agents lipopolysaccharide (LPS) and muramyl dipeptide (MDP) interact with osteoblasts, their effect on the synthesis of collagenase and tissue inhibitor or metalloproteinases (TIMP) from monolayer cultures of mouse osteoblast-like cells was investigated. All concentrations of LPS (0.1, 1.0 and 10.0 micrograms/ml) significantly stimulated collagenase levels compared to unstimulated controls. This suggests that LPS, like hormonal stimulators of bone resorption, interacts with osteoblasts. In contrast, MDP (0.01, 0.1 and 1 microM) did not significantly stimulate collagenase or TIMP levels, indicating that MDP may not interact with osteoblasts. Possible alternative mechanisms of MDP-mediated bone resorption are discussed.
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PMID:The effect of lipopolysaccharide from bacteroides gingivalis and muramyl dipeptide on osteoblast collagenase release. 254 Aug 90

Collagenolytic enzyme release from bone cells was studied using cultured calvarial cells which are capable of degrading calcified and noncalcified collagen (cells from normal mice) or only noncalcified collagen (cells from osteopetrotic (mi/mi) mice). Treatment of cells from either normal or mi/mi mice with parathyroid hormone (PTH) or lipopolysaccharide (LPS) resulted in the appearance of latent collagenolytic enzyme activity in the medium. Chromatography of media from cells from normal mice treated with PTH on lysine-Sepharose resulted in the separation of latent collagenase and latent gelatinase. Further characterization of the enzymes showed that they were similar to those previously isolated from media of calvaria cultured with heparin. Collagenase activity of media of cells from normal or mi/mi mice treated with PTH or LPS yielded identical elution patterns upon chromatography on lysine-Sepharose. These results show that the mi allele has no effect on regulation of latent collagenolytic enzyme release. The results show that the mi allele has no effect on regulation of latent collagenolytic enzyme release. The data also suggest that previously described differences between PTH- and LPS-stimulated collagen degradation in cultured calvaria are due to factors other than differences in the ability of these agents to stimulate the release of collagenolytic enzymes.
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PMID:Stimulation of collagenolytic enzyme release from cultured bone cells of normal and osteopetrotic (mi/mi) mice by parathyroid hormone and lipopolysaccharide. 254 66

Inflammation plays an important role in homeostasis of the body. We therefore can assume that an inflammatory state occurs during ontogenesis of animals. To address this problem, we examined the ability of tumor necrosis factor (TNF), one of the inflammatory mediators, to be secreted by mouse cells during development. We cultured cells prepared from various parts of fetuses (10-19 days of gestation) and postnatal brains by collagenase digestion and assayed the secreted TNF activity by the L-929 cytotoxicity test. We found TNF activity by fetal cells without any stimulation. The spontaneous secretion of TNF was relatively high at around 13-15 days of gestation. The secretion was enhanced by lipopolysaccharide (LPS), showing that fetal cells are in an activated state for TNF secretion. These TNF activities were neutralized completely by rabbit anti-murine TNF antibody. Spontaneous and LPS-enhanced secretion by postnatal brain cells reached a peak around 7 days after birth, and thereafter declined rapidly. This time course was well correlated to the increase in the weight of brain. The producing cells were negative in macrophage marker surface antigen, and heterogeneous in relation to adherence and phagocytic activity, showing that TNF is secreted by various types of cells in the fetal body. These results suggest the presence of an inflammation-like state during ontogenesis. We consider that this "ontogenic inflammation" may be the prototype of inflammation, which can regulate homeostasis of the adult body.
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PMID:Secretion of tumor necrosis factor during fetal and neonatal development of the mouse: ontogenic inflammation. 260 Jun 4

The possible role of liver parenchymal cells in the uptake and degradation of bacterial lipopolysaccharide (LPS) was investigated in vitro by employing radiolabelled LPS as substrate. Hepatocytes obtained from Wistar rats by collagenase treatment were found to take up LPS only when it was not linked to the polysaccharide of O-antigen. The amount of LPS taken up increased with time and after 48 h incubation it increased in a dose-dependent manner up to at least 30 micrograms. When incubated with LPS radiolabelled exclusively in the fatty-acid moiety, cultured hepatocytes released lipophilic materials into the culture medium. These were identified as beta-hydroxytetradecanoic acid and triglyceride, in the ratio of 7:I. These results indicate that the R-form of LPS which lacks the O-antigen polysaccharide is taken up and deacylated in hepatocytes, and the derived fatty acids are released into the culture medium either in the free form or after conversion to triglyceride.
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PMID:Deacylation of bacterial lipopolysaccharide in rat hepatocytes in vitro. 266 23

The process of uptake of endotoxin by cells of the reticuloendothelial system is of current interest. Rabbit peritoneal macrophages have been used to study macrophage-endotoxin interactions and have suggested a receptor-mediated process. It is generally believed that the site of in vivo endotoxin clearance is the liver and that this clearance involves the Kupffer cell population. In the current report, the uptake characteristics of iodine-125-labeled Salmonella minnesota lipopolysaccharide (LPS) were compared in both isolated rat Kupffer cells and elicited rat peritoneal cells. Both types of cells were isolated from male Sprague-Dawley rats fed a semisynthetic AIN-76 5% saturated-fat diet either by peritoneal lavage for peritoneal cells or by collagenase perfusion followed by purification on a 17.5% metrizamide gradient for Kupffer cells. Hot phenol water-extracted S. minnesota LPS was labeled with iodine by the chloramine-T method following a reaction with methyl-p-hydroxybenzimidate. The in vitro uptake of [125I]LPS by Kupffer cells was unsaturable up to concentrations of 33.33 micrograms/ml, while peritoneal cells became saturated at between 16.67 and 25 micrograms of LPS per ml. Uptake by both types of cells could be inhibited by a 10-fold excess of unlabeled LPS. Kinetic experiments demonstrated that Kupffer cells were unsaturable after 60 min of incubation, while peritoneal cells were saturable after 40 min of incubation. Pretreatment with 75 mM colchicine inhibited uptake by peritoneal cells but not Kupffer cells, while pretreatment with 12 mM 2-deoxyglucose inhibited uptake by Kupffer cells but not peritoneal cells. These results are consistent with a process of receptor-mediated endocytosis for peritoneal cells, while Kupffer cells may internalize endotoxins by absorptive pinocytosis. These results suggest that studies of peritoneal cell-endotoxin interactions do not accurately describe the physiologic process within the liver, the major site for the clearance of gut-derived endotoxins.
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PMID:Comparative studies of endotoxin uptake by isolated rat Kupffer and peritoneal cells. 282 79

Uterine cervical explants in culture from pregnant rabbits at term spontaneously synthesized and secreted three species of interleukin-1-like factors in culture medium. The addition of the exogenous mitogen lipopolysaccharide to the culture system induced further release of these factors. However, these phenomena were not observed with explants from nonpregnant cervices. The molecular weights of these factors estimated by gel filtration were approximately 49, 22, and 12 kDa, respectively, and were identical to those of interleukin-1 from rabbit macrophages and polymorphonuclear leukocytes. These results indicate that interleukin-1-like factors are involved in cervical ripening and dilatation, especially in the acceleration of collagenase production, at term.
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PMID:Spontaneous production of interleukin-1-like factors from pregnant rabbit uterine cervix. 283 85

Guinea pig Kupffer cells were obtained by partial digestion of the liver with pronase and collagenase and purified by centrifugal elutriation. Cells were kept in monolayer culture and their capacity to secrete superoxide anion in response to phagocytosis of zymosan was determined by the cytochrome c method. Compared to resident peritoneal macrophages, Kupffer cells produced somewhat less superoxide (60% +/- 30%). Both cell types were activated by 24 h preincubation with lipopolysaccharide from Salmonella minnesota or muramyl dipeptide to give twice as high a superoxide response to zymosan. The same effect was achieved when Kupffer cells in vitro were incubated for 3 days with supernatants from phytohaemagglutinin-activated peripheral T lymphocytes or recombinant gamma-interferon. These data demonstrate that the resident macrophages of the liver, the Kupffer cells, are able to increase their capacity to secrete reactive oxygen intermediates after proper activation; this fact is possibly important in the pathogenesis of hepatocyte damage upon inflammatory reactions in the liver.
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PMID:Guinea pig Kupffer cells can be activated in vitro to an enhanced superoxide response. I. Comparison with peritoneal macrophages. 285 90

The objective of these studies was to characterize some aspects of collagenase production by rabbit articular chondrocytes cultured with stimulated monocyte supernatants. Supernatants from human monocytes stimulated with 20 ng/ml bacterial lipopolysaccharide (LPS) induced the synthesis and secretion of latent collagenase by the chondrocytes beginning at 6 hr. The time course and dose response of collagenase production by the chondrocytes were identical using crude monocyte supernatants or semipurified interleukin 1 (IL-1). Recombinant or purified human interleukin 2 failed to induce collagenase production in the cultured chondrocytes. The response of the chondrocytes was inhibited by actinomycin D or cycloheximide and not by corticosteroids. Phorbol myristate acetate (PMA) alone failed to directly stimulate the chondrocytes. However, PMA led to enhanced collagenase production by chondrocytes when incubated with submaximal amounts of LPS-stimulated monocyte supernatant or semipurified IL-1. LPS alone in amounts between 0.1 and 10.0 micrograms/ml directly stimulated collagenase production in chondrocytes between 4 and 11 days in culture. These data confirm those of other laboratories that IL-1 may be the active factor in monocyte supernatants responsible for inducing collagenase production in cultured chondrocytes. Further characterization of this response indicates that the collagenase is not preformed in the cells and stimulation of its production is not inhibited by corticosteroids. Cell supernatants or IL-1 preparations containing PMA as low as 1.0 ng/ml or LPS as low as 1.0 microgram/ml may give falsely high values for IL-1 activity when assayed by stimulation of collagenase production in cultured chondrocytes.
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PMID:Characteristics of chondrocyte responses to a human interleukin 1-like factor. 299 Jul 84

Human macrophages have been implicated in connective tissue remodeling; however, little is known about their direct effects upon collagen degradation. We now report that human alveolar macrophages in culture produced both a collagenase and a collagenase inhibitor. The collagenase was secreted in latent form and could be activated by exposure to trypsin. Collagenase production could be increased three- to fourfold by incubating the cells with lipopolysaccharide, but synthesis was largely unaffected by exposure to phorbol myristate acetate. By several criteria, macrophage collagenase was the same as the collagenase secreted by human skin fibroblasts: (a) they were antigenically indistinguishable in double immunodiffusion; (b) both degraded type III collagen preferentially to type I, had little activity against type II collagen, and none against types IV and V, and (c) their affinity for susceptible collagens was equivalent, Michaelis constant = 1-2 microM. Collagenase inhibitory activity was also present in the macrophage-conditioned medium, and was accounted for by an antigen that showed immunologic and functional identity with the collagenase inhibitor secreted by human skin fibroblasts. The amount of inhibitor released by unstimulated cells, approximately 100 ng/10(6) cells per 24 h, was substantially augmented by both phorbol and lipopolysaccharide, although considerable variability in response to these agents was observed between macrophage populations derived from different subjects. As negligible quantities of collagenase or collagenase inhibitor were detectable intracellularly, it appeared that both proteins were secreted rapidly after synthesis. Thus, human macrophages have the capacity to modulate collagen degradation directly by production of collagenase and collagenase inhibitor.
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PMID:Human alveolar macrophages produce a fibroblast-like collagenase and collagenase inhibitor. 299 37

Although the fibrosis observed during chronic liver injury is the result of a complex process, the striking accumulation of collagen in end stage liver disease has provoked interest in the mechanisms that regulate both collagen production and degradation in the diseased liver. The present studies have examined the cell interactions that may be important in the regulation of collagen degradation. Although minimal amounts of interstitial collagenase activity were noted in cultures of normal hepatocytes and sinusoidal cells, the co-cultures of these cells in the presence of lipopolysaccharide showed a substantial increase in collagenase activity. When the hepatocytes were obtained from rats that had been treated with carbon tetrachloride in vivo, the enhanced activity seen in the co-cultures did not require the addition of lipopolysaccharide. Further characterization of this interaction suggested that the increase in collagenolytic activity was partially due to the elaboration of soluble factors by the hepatocyte, which stimulated collagenase production by the sinusoidal cell population. Elaboration of collagenase activity by the sinusoidal cells was inhibited by cycloheximide, suggesting that protein synthesis was required. The proteolytic activity was abrogated by inhibitors of metalloproteinases but not by serine or thiol proteinase inhibitors. The degradation products of type I collagen were typical of the expected products seen with vertebrate collagenases. Thus, it appears that the increased collagenolytic activity detected in this co-culture system is attributable to the production of interstitial collagenase by the sinusoidal cell population. Such cell-cell interactions may play an important role in the maintenance of normal connective tissue structure of the liver during disease processes.
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PMID:Stimulation of interstitial collagenase in co-cultures of rat hepatocytes and sinusoidal cells. 300 4


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