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)

Antigen 60 (A60) is the main thermostable immunogen of both 'old tuberculin' (OT) and 'purified protein derivative' (PPD), known reagents for cutaneous tests in tuberculosis. It is recognized by bidimensional immunoelectrophoresis with anti-BCG antiserum, where it appears as the less mobile component. A60 was prepared from the cytoplasm of Mycobacterium bovis BCG, and purified by exclusion gel chromatography and lectin affinity chromatography. Labelled A60 was obtained by radioiodination and used for a radioimmunoassay. Composition of A60 was explored by use of organic solvents, chemicals and enzymes. It contained two fractions of free and bound lipids, as well as protein and polysaccharide moieties. After removal of both free and bound lipid fractions, the core still retained the ability to form immunoprecipitinogen lines with anti-BCG antiserum. The lipopolysaccharide and lipo-protein moieties of A60, as well as the free lipid fraction, were also complexed by antibodies. It is concluded that A60 is a lipopolysaccharide-protein complex of 10(6) to 10(7) daltons, which is a major immunogenic component of mycobacterial cytoplasm. The detailed structure of this antigen, its immunological properties, and its use for an ELISA type immunoassay for tuberculosis are described in two other publications.
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PMID:Preparation and properties of antigen 60 from Mycobacterium bovis BCG. 354 72

A monoclonal antibody is described that was generated by immunizing mice with cultured human blood monocytes. The antibody (27E10) belongs to the IgG1 subclass and detects a surface antigen at Mr 17,000 that is found on 20% of peripheral blood monocytes. The antigen is increasingly expressed upon culture of monocytes, reaching a maximum between days 2 and 3. Stimulation of monocytes with interferon-gamma (IFN-gamma), 12-O-tetradecanoyl-phorbol-13-acetate (TPA), and lipopolysaccharide (LPS) but not with N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP) increased the 27E10 antigen density. The amount of 27E10-positive cells is not or is only weakly affected. The antigen is absent from platelets, lymphocytes, and all tested human cell lines, yet it cross-reacts with 15% of freshly isolated granulocytes. By using the indirect immunoperoxidase technique, the antibody is found to be negative on cryostat sections of normal human tissue (skin, lung, and colon) and positive on only a few monocyte-like cells in liver and on part of the cells of the splenic red pulp. In inflammatory tissue, however, the antibody is positive on monocytes/macrophages and sometimes on endothelial cells and epidermal cells, depending on the stage and type of inflammation, e.g., BCG granulomas are negative, whereas psoriasis vulgaris, atopic dermatitis, erythrodermia, pressure urticaria, and periodontitis contain positively staining cells. In contact eczemas at different times after elicitation (6 hr, 24 hr, and 72 hr), the 27E10 antigen is seen first after 24 hr on a few infiltrating monocytes/macrophages, which increase in numbers after 72 hr. From this it is concluded that the antibody 27E10 detects an antigen expressed by a subset of peripheral blood monocytes. In situ the antigen is found only in inflammatory tissues and is absent from normal resident mononuclear phagocytes.
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PMID:A monoclonal antibody to a subset of human monocytes found only in the peripheral blood and inflammatory tissues. 372 15

A hybridoma clone secreting rat monoclonal antibody (MAB) designated as 3F3.5F and which reacted with a population of activated tumoricidal mouse peritoneal macrophage (M phi) was produced by the fusion of mouse myeloma cells with rat spleen cells immunized against adherent BCG-activated mouse peritoneal exudate cells (adherent BCG-PEC). The antibody was cytotoxic and of the rat IgM class. The specific reactivity of the antibody with mouse primary cells and cell lines was examined by complement-dependent cytotoxicity and indirect immunofluorescence flow cytometry analysis. The antibody was found to bind to about 40% of the adherent BCG-PEC activated in vivo and elicited peritoneal macrophages activated in vitro by lymphokine and lipopolysaccharide (LPS), to about 35% of polymorphonuclear neutrophils (PMN) 15 hr after intraperitoneal injection of BCG, to about 30% of bone marrow cells from BCG-infected mice, to about 10% of P815 mastocytoma cells and to thioglycollate-induced PEC to some degree. It did not bind to other cells tested including BCG-induced peritoneal lymphocytes, non-tumoricidal PEC, thymocytes, spleen cells, resting bone marrow cells from normal mice, lymphomas, myelomas, fibroblasts, or macrophage-cell lines. Pretreatment of adherent BCG-PEC with MAB 3F3.5F and rabbit complement caused a considerable decrease in tumor cytotoxicity toward P815 cells, but the same pretreatment of non-adherent BCG-PEC had no inhibitory effect on natural killer activity for YAC-1 cells.
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PMID:A novel rat monoclonal antibody directed against a population of activated mouse peritoneal macrophages. 374 66

A synthetic compound (506), beta (1-6) D-glucosamine disaccharide 1,4'-bisphosphate, which is acylated at 2'-amino and 3'-hydroxyl groups with (R)-3-dodecanoyloxytetradecanoyl and (R)-3-tetradecanoyloxytetradecanoyl groups, respectively, and has (R)-3-hydroxytetradecanoyl groups at 2-amino and 3-hydroxyl groups, exhibited full endotoxic activities identical to or sometimes stronger than those of a reference lipid A from an Escherichia coli Re-mutant (strain F515). Endotoxic activities tested include pyrogenicity and leukopenia-inducing activity in rabbits, body weight-decreasing toxicity in normal mice, lethal toxicity in galactosamine-sensitized mice and chicken embryos, and the preparation and provocation of the local Shwartzman reaction in rabbits. Compound 406, a synthetic counterpart of a biosynthetic precursor of lipid A molecule, showed by contrast only weak activities in all of the above assay systems except for the lethality in galactosamine-loaded mice. This finding strongly suggests that the presence of acyloxyacyl groups at the C-2' and C-3' positions of the disaccharide backbone is one of the most important determinant structures of the lipid A molecule for exhibition of strong biological activities characteristic of lipopolysaccharide and its lipid A moiety. The activities of the corresponding 4'-monophosphate (compound 504) and 1-monophosphate (505) analogs were considerably less than those of the parent molecule 506 and the reference F515 lipid A. Regarding other biological activities, not only compound 506 but also compounds 504, 505, and 406 showed definite activities, sometimes comparable to those of F515 lipid A and other reference natural products. These are the activation of Tachypleus tridentatus amoebocyte clotting enzyme cascade and human complement via the classical pathway, mitogenic and polyclonal B-cell activation of murine splenocytes, stimulation of peritoneal macrophages in a guinea pig, enhancement of migration of human blood polymorphonuclear leukocytes, and induction of a serum factor that is cytostatic and cytocidal to L-929 cells in Mycobacterium bovis BCG-primed mice. Relative potencies of test synthetic compounds depended on the assay systems and varied from one system to another. Dephospho-compound 503 lacked most of the biological activities that were definitely observed with phosphorylated compounds, probably because of its insolubility. This study demonstrates the successful chemical synthesis of an E. coli-type lipid A.
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PMID:Synthetic lipid A with endotoxic and related biological activities comparable to those of a natural lipid A from an Escherichia coli re-mutant. 389 27

The faster degradation of antigen by macrophages in Biozzi low (L) responder mice, compared to Biozzi high (H) responder mice, is thought to be responsible for their lower antibody response. We have measured four functions associated with macrophages to see whether macrophages from L mice were generally more active than those from H mice. Peritoneal macrophages obtained from normal mice were compared with those from groups of mice given Mycobacterium bovis BCG or Propionibacterium acnes. Cells from normal H mice gave a stronger oxidative burst when triggered with phorbol myristate acetate, and were more cytotoxic for tumour cells than cells from L mice. Cells from all mice injected with BCG or P. acnes gave a stronger oxidative burst, and were more cytotoxic for tumour cells; again, both responses were higher in H mice than in L mice. By contrast, when groups of mice that had received P. acnes were given endotoxin and bled, higher titres of tumour necrosis factor were found in the sera of L mice. Spleen cells from both lines of mice released similar levels of interleukin-1, both spontaneously and in response to lipopolysaccharide. Our results suggest that these various macrophage responses are expressed independently in H and L mice.
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PMID:Macrophage functions in Biozzi mice. 389 22

The growth of tubercle bacilli in serum samples of untreated animals depends upon the availability of ionic iron which serves as a growth factor in supporting bacillary multiplication. The amount of available iron in serum is determined by the ratio between iron-saturated and iron-free transferrin; a low value for the ratio is associated with tuberculostasis (e.g., human serum, 0.4), whereas a high value is associated with the growth-supporting quality (e.g., guinea pig serum, 5.6). The treatment of guinea pigs with lipopolysaccharide of Escherichia coli or tuberculous cell wall material consistently and significantly reduced serum iron levels; a similar but less striking effect was observed in BCG-vaccinated animals. Pronounced differences were observed in the time of appearance and duration of serum hypoferremia; in lipopolysaccharide-treated animals, it appeared in 1 day and lasted for several days, whereas in BCG-vaccinated animals it appeared in about 2 weeks and lasted for much longer time periods. The induced hypoferremia was always associated with the concomitant development of serum tuberculostasis which could be neutralized by the addition of iron. These results indicate, therefore, that the mechanism of induced serum tuberculostasis in lipopolysaccharide- or tuberculous cell wall-treated and BCG-vaccinated guinea pigs is the same as that present in tuberculostatic sera of untreated animals.
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PMID:Mechanism of tuberculostasis in mammalian serum. II. Induction of serum tuberculostasis in guinea pigs. 489 10

C3H/HeJ mice exhibit a marked insensitivity to bacterial lipopolysaccharide (LPS) in vivo. Pretreatment of these mice with viable BCG organisms 11 days before LPS administration renders them sensitive to the lethal effects of a highly purified, phenol-extracted LPS. Other in vivo responses to LPS are increased in BCG-infected C3H/HeJ mice in parallel with enhanced lethality. These include 1) the elevation of serum interferon, 2) the production of the acute phase reactant, serum amyloid A (SAA), and 3) hypoglycemia. However, BCG infection has only a minimal effect on anti-LPS antibody production. BCG-infected C3H/HeJ mice approach the LPS sensitivity of normal C3H/HeN mice, but the enhanced LPS sensitivity is transient and decreases over a 2-month period. The ability of BCG to induce LPS sensitivity in C3H/HeJ mice demonstrates that LPS unresponsiveness is not due to an absolute defect in this strain, but rather, a partially reversible state of hyporesponsiveness. In addition, these findings, in conjunction with other observations, suggest that the enhancement of LPS sensitivity induced by BCG infection is mediated primarily through an effect on T cells and/or macrophages rather than B lymphocytes.
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PMID:BCG-induced enhancement of endotoxin sensitivity in C3H/HeJ mice. I. In vivo studies. 615 89

An antiserum to immune T-type mouse interferon was prepared in rabbits by repeated injections of interferon, induced by phytohaemagglutinin (PHA) in mouse spleen cells and purified to 1 X 10(5) units/mg protein. The antiserum neutralized mouse interferons synthesized in vitro in response to several T mitogens and Brucella organisms, and also the type II interferon present in the serum of BCG-sensitized mice after an injection of the specific antigen, tuberculin. All these interferons are thus antigenically related; they are also all unstable at pH 2. In contrast, the antiserum did not neutralize interferons induced by West Nile virus (WNV) and Newcastle disease virus (NDV) in vitro, or by lipopolysaccharide and Brucella organisms in vivo; all these interferons are stable at pH 2. It also failed to neutralize a non-glycosylated virus interferon prepared in the presence of tunicamycin.
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PMID:Production of antibodies against mouse immune T (type II) interferon and their neutralizing properties. 616 Feb 1

The time course of development and decline of the ability of BCG-infected mice to produce interferon in the serum in response to the intravenous infection of purified protein derivative of tuberculin (PPD) was very similar to that of their systemic hypersensitivity to PPD. A cytotoxic factor (cytotoxin) was produced in parallel with interferon in the serum of BCG-infected mice after stimulation with PPD. The duration of the period in which cytotoxin-production responsiveness to PPD was definitely detectable was much shorter than that for interferon-production responsiveness although the periods for the maximum production of interferon and cytotoxin coincided. The kinetics of release of interferon in the serum of BCG-infected mice after stimulation with PPD did not parallel that of release of cytotoxin. The four kinds of activities, interferons and cytotoxins induced by PPD and lipopolysaccharide (LPS) in the serum of BCG-infected mice, were compared for their stability to heating at 56 C and to treatment at pH 2. The kinetics of inactivation of these four activities differed significantly, when the serum was either heated at 56 C or treated at pH 2. Interferon produced in response to LPS could be neutralized by anti-L cell(NDV) interferon rabbit serum as easily as L cell (NDV) interferon, 16 times as much antiserum was required to neutralize the same amount of interferon in response to PPD, but cytotoxins induced by PPD and LPS were not neutralized at all by the antiserum. From these findings it is thought likely that interferons and cytotoxins induced by PPD and LPS in the serum of BCG-infected mice are different substances, although the antigenic relationship between cytotoxins induced by PPD and LPS remains unknown.
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PMID:Interferon and cytotoxic factor (cytotoxin) released in the blood of mice infected with Mycobacterium bovis BCG. III. Interferon and cytotoxin induced by the specific antigen as compared with those induced by bacterial lipopolysaccharide. 616 45

Variations exist between different strains of inbred mice in the release of lymphokines into the circulation. A number of manifestations of cell-mediated immunity in mice sensitized intravenously with Mycobacterium bovis BCG were analyzed to determine their association with the in vivo release of gamma interferon (IFN-gamma) and migration inhibitory factor. Differences occurred among the strains in the proliferative responses of splenic cells to specific antigen and in the release of IFN after the challenge of BCG-sensitized mice with lipopolysaccharide. However, the capacity of an individual strain to release migration inhibitory factor and IFN-gamma into the circulation did not parallel the extent either of the proliferative responses or of the release of IFN induced by lipopolysaccharide. Not all of the strains developed marked delayed footpad reactions to challenge with PPD regardless of the extent of their responses by other parameters. Delayed footpad reactions did develop in mice sensitized via the subcutaneous route, although this sensitization did not result in the capacity to release migration inhibitory factor and IFN-gamma into the circulation of individual inbred strains.
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PMID:Mechanisms in the in vivo release of lymphokines: relationship of high and low responsiveness to other parameters of the immune response. 617 May 85


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