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 effects of inhibitors of cell division on polyclonal stimulation induced either by bacterial lipopolysaccharide (LPS) or by a synthetic adjuvant, MDP, were compared, using different target cells. Doses of colchicine that prevented 3H-thymidine incorporation also prevented the induction of antibodies against TNP and against an altered self antigen: bromelain-treated mouse red blood cells (br-MRBC). Under identical conditions, incubation with cytosine arabinoside (CA) strongly prevented the induction of anti-TNP PFC and to a lesser degree anti-SRBC PFC. However, the number of anti br-MRBC PFC was unchanged even when a dose of CA which inhibits totally the incorporation of 3H-thymidine was used. Our findings indicate that the general term "polyclonal stimulation" may concern at least two different types of cell populations and therefore we strongly stress the importance of choosing similar targets in comparative experiments.
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PMID:Effect of cell division inhibitors on polyclonal activation can vary according to the target cell used. 39 5

The combined effects of the synthetic glucosaminylmuramyl dipeptide (GMDP) on the antitumor activity of chemically synthesized lipid A analogs, compound A-103 (glucosamine-4-phosphate with (R)-3-tetradecanoyloxytetradecanoyl group at the C-2 and C-3 positions), Escherichia coli-type lipid A (506), Salmonella typhimurium LT-2 lipopolysaccharide (LPS) against Meth A fibrosarcoma in mice were examined. Meth A fibrosarcoma cells (5 x 10(5) were inoculated intradermally into BALB/c mice on day 0, and compound A-103 and/or GMDP was administered intravenously (i.v.) on days 7 and 9. Two i.v. injections of A-103 (50 micrograms) alone or GMDP (10 micrograms) alone induced 42.8 or 51.8% inhibition of the rate of tumor growth, however, A-103 (100 micrograms) with GMDP (10 micrograms) exhibited a high 68.7% inhibition rate 19 days after tumor inoculation. The inhibition of the tumor growth rate by the combination A-103 (100 micrograms) or 506 (50 micrograms) with GMDP (10 micrograms) was stronger than that of A-103 or 506 with MDP (10 micrograms). The combination of LPS (1 or 10 micrograms) with GMDP (10 micrograms) exhibited a higher inhibition rate than that of LPS with MDP, and three or four tumor-free mice out of five mice were observed, suggesting that the combined effect of GMDP is more potent than that of MDP. With the addition of GMDP, A-103 did not enhance the production of tumor necrosis factor (TNF) on the basis of L929 cell lysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Combined effects of synthetic lipid A analogs or bacterial lipopolysaccharide with glucosaminylmuramyl dipeptide on antitumor activity against Meth A fibrosarcoma in mice. 146 73

We recently reported hyperproduction of interleukin-1 (IL1) and hyperexpression of IL1 beta mRNA, after in vitro activation by lipopolysaccharide (LPS) in peripheral macrophages of several neurological mutant mice, i.e. staggerer, lurcher, pcd and reeler, that exhibit patterns of neuronal degeneration in the cerebellum; in the present study, we investigated the expression of several cytokine mRNA in peripheral macrophages of other mutants with neuronal degeneration in the cerebellum or in the spinal cord to determine whether this genetic dysregulation is specific for IL1 beta or whether it reflects a generalized hyperexcitability of these macrophages. Hyperexpression of IL1 beta mRNA was present in the cerebellar mutants nodding and nervous, but not in weaver. A similar phenomenon was found, but to a lesser extent, in the spinal mutants dystonia musculorum, wobbler and motor neuron degeneration. On the contrary, no hyperexpression of IL1 beta mRNA was found in non-genetic models of neuronal degeneration (Wistar rats treated with X irradiation or with 3-acetyl-pyridine). In the heterozygote staggerer +/sg, which exhibits a late onset of cerebellar neuronal loss, hyperexpression was found not only in 12-month old animals but also in 2-month old ones, i.e. when the number of cerebellar neurons is still normal. Synthetic molecules (muramyl dipeptides) like MDP or murabutide (Mu), known as macrophage activators, were also efficient in inducing IL1 hyperexpression in sg/sg macrophages. Hyperexpression of two other cytokine mRNA, i.e. IL1 alpha and tumour necrosis factor alpha mRNA, was also detected in LPS-stimulated macrophages of staggerer and lurcher mutant mice. These data led us to conclude that the macrophages of spinal and cerebellar mutants are in a state of general hyperexcitability. Work is in progress to establish whether the cytokine abnormalities result from a defect intrinsic to the macrophages of the mutant mice or are secondary to the degenerative process ultimately leading to neuronal loss.
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PMID:Peripheral macrophage abnormalities in mutant mice with spinocerebellar degeneration. 156 42

Increased secretion of H2O2, O2- and lysozyme by human monocytes in vitro on treatment with cisplatin, rIFN-Y (interferon-Y), LPS (lipopolysaccharide) and MDP (muramyl dipeptide) is reported. It is suggested that increased production of these secretory products represent the activated state of monocytes. These in vitro activated monocytes could either kill the tumor cells via increased contact mediated cytolysis or cytolysis mediated via the release of the secretory products like H2O2, O2- and lysozyme.
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PMID:Effect of cisplatin, rIFN-Y, LPS and MDP on release of H2O2, O2- and lysozyme from human monocytes in vitro. 166 47

The phagocytic, oxygen free radical generating and cytotoxic activities of macrophages from C57BL/6J mice fed either a normal or an atherogenic high-fat diet have been investigated. Phagocytosis of aggregated low density lipoprotein (LDL) was only slightly inhibited by the high-fat diet although phorbol myristate acetate (PMA)-induced hydrogen peroxide (H2O2) and superoxide anion (O2-) production was significantly reduced. Activation of tumoricidal activity against L929 target cells by lipopolysaccharide (LPS) or lymphocyte-derived macrophage-activating factor (MAF), but not N-acetylmuramyl-L-alanyl-D-isoglutamine (MDP), was also significantly reduced in macrophages from mice fed the high-fat diet. These results indicate that an atherogenic diet is capable of significantly affecting the responsiveness of macrophages to a number of stimulatory agents which act via specific membrane receptors.
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PMID:The effect of a high-fat diet on murine macrophage activity. 205 Apr 36

Acute anterior uveitis in man is related to Gram negative bacterial infection occurring at sites distant to the eye. This could involve intraocular localization of inflammatory bacterial cell wall constituents. Modulation of the blood-aqueous barrier in rabbit and rat, by muramyl dipeptide (the monomer of peptidoglycan) and lipopolysaccharide (and its monomer lipid A) was studied. The rabbit eye was found to be highly susceptible to MDP and LPS, although without cellular infiltration. In contrast the rat eye was demonstrated to be totally refractory to MDP. The response to LPS in the rat was modest, required high dosages and ocular changes were slow to occur, but cellular infiltration was readily apparent. Since MDP is found in Gram positive (as well as Gram negative) bacterial cell walls it is hypothesized that Gram positive bacteria might also play a role in causing uveitis in man.
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PMID:Modulation of the blood-aqueous barrier by gram positive and gram negative bacterial cell wall components in the rat and rabbit. 231 81

Alveolar macrophages (AM) freshly obtained by bronchoalveolar lavage suppressed significantly, in a dose-dependent fashion, lung interstitial lymphocytes cytotoxicity against the NK-sensitive target cells, YAC-1. Kinetic experiments revealed that AM-mediated suppression of NK activity was seen following short-term incubation of AM with lymphocytes (4 h) and was unchanged after a 24 h co-culture period. Freshly obtained lung lymphocytes and lymphocytes incubated for 24 h were similarly inhibited by AM. In addition, incubation of AM for 24 h did not abrogate their suppressive effect on lung NK activity. Interestingly, AM-conditioned media, also caused a significant inhibition of lung NK activity. Furthermore, in vitro activation of AM with lipopolysaccharide (LPS, 5 micrograms/ml) and muramyl dipeptide (MDP, 20 micrograms/ml) significantly enhanced the inhibitory effect of AM on lung NK activity. Similarly, in vivo activation of AM locally by intratracheal instillation of attapulgite, an inflammatory agent, resulted in greater AM-mediated down regulation. Taken together, these data indicate that lung NK activity is modulated by locally derived factors and suggest that pharmacologic manipulation of AM may play a determining role in the activation of lung NK activity by biological response modifiers (BRM).
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PMID:Modulation of lung-associated natural killer activity by resident and activated alveolar macrophages. 233 60

Peritoneal exudate macrophages from mice, rats, and guinea pigs were assessed using six different parameters of macrophage activation to determine whether the cells were stimulated under similar experimental conditions. Peritoneal exudate macrophages from mice, irrespective of strain, were far less responsive to a variety of in vitro stimulatory effects of N-acetylmuramyl-L-alanyl-D-isoglutamine than those from rats or guinea pigs, while no significant differences were noted with the reactivity to stimulation by endotoxic lipopolysaccharide. We conclude that macrophage activation by MDP in vitro is species dependent.
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PMID:Lack of response of murine peritoneal macrophages to in vitro activation by muramyl dipeptide (MDP). I. Macrophage activation by MDP is species dependent. 235 99

Human blood monocytes isolated by centrifugal elutriation from healthy donors were tested for ability to produce membrane-associated IL-1 in response to activation stimuli such as various types of interferons (alpha, beta and gamma) and/or synthetic des-methyl muramyl dipeptide (norMDP). When monocytes were treated with norMDP or lipopolysaccharide (LPS) for 16 hr, they released IL-1 into their culture supernatant. When these activated monocytes were fixed with paraformaldehyde (PFA), they stimulated blastogenic responses of C3H/HeJ mouse thymocytes to PHA, suggesting that membrane-associated IL-1 could be induced by norMDP or LPS. Membrane-associated IL-1 was also found to be induced by the synergistic actions of suboptimal concentrations of rIFN-gamma and nor MDP, but not of rIFN-alpha A or rIFN-beta with norMDP. A specific anti-IL-1 alpha antiserum completely inhibited membrane-associated IL-1 activity, but did not affect the thymocyte-stimulating activity of fixed monocytes. IL-1 alpha was detected by fluorescence staining using the anti-IL-1 alpha antiserum on monocytes fixed after gamma IFN-gamma and norMDP. These results suggest that IFN-gamma may be important in expression of membrane-bound IL-1 alpha by the human blood monocytes responsible for regulation of immune responses in vivo.
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PMID:Induction of membrane-associated interleukin 1 alpha (IL-1 alpha) by synergistic activation of human blood monocytes with interferon gamma and muramyl dipeptide analog. 248 23

We investigated the effects of the active principle of lipopolysaccharide (LPS), synthetic lipid A (compound 506), and of its related compounds GLA-60, -59 and -27, on murine macrophage activation and cytokine induction. GLA-60, which is devoid of endotoxic activity, showed interleukin-1 (IL-1)-inducing activity and activation of murine macrophages comparable to those of LPS or compound 506. The biological activities of six conjugates of GLA-60 with MDP derivatives GMD-323 to -328 were investigated in this study. All the GMD compounds except GMD-323 showed potent inducing activities for IL-1 and tumoricidal macrophages, especially GMD-324 and -326, which exhibited much higher activity than GLA-60. However, TNF- and CSF-inducing activities of these conjugates were lower than those of GLA-60. IL-1-inducing activity of the mixture of MDP derivative (GMD-267) and GLA-60 was higher than that of the conjugates (GMD-324) or that of GLA-60 and GMD-267 alone.
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PMID:Adjuvant activities of synthetic lipid A subunit analogues and its conjugates with muramyl dipeptide derivatives. 267 86


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