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

The effects of carbon dust inhalation on the bone marrow-derived (B) and thymus-derived (T) lymphocyte populations of spleen and mediastinal lymph node (MLN) cultures were examined. The concanavalin A (Con A)-responsive cell population (T cells) in the spleen was found to be depressed after 7 days of pre-exposure to carbon dust. However, this effect was transient, and after 14, 21, and 28 days of pre-exposure to carbon dust, the Con A-responsive cells exhibited a 30 to 40% enhancement over control group responses. Conversely, Con A-responsive cells in the pooled MLN cultures exhibited depression, ranging from 22 to 33% below control group values, after 7, 14, and 28 days of pre-exposure to carbon dust. The lipopolysaccharide (LPS)-responsive cell population (B cells) in the spleens of carbon-exposed mice was found not to differ significantly from control group values after all times of pre-exposure. LPS-responsive cells in the MLN cultures exhibited enhancement, ranging from 49 to 74% above control values, after 14, 21, and 28 days of pre-exposure to carbon dust. The ability of carbon spleen cell cultures from carbon-exposed mice to undergo antigen induced blast transformation after sensitization with Mycobacterium tuberculosis H37Ra was also determined. Mice exposed to carbon dust inhalation 2 weeks before and 3 weeks after aerosol or subcutaneous immunization exhibited significantly enhanced ratios of transformation upon culture of their spleen lymphocytes with purified protein derivative of tuberculin.
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PMID:Effects of carbon dust inhalation on the cell-mediated immune response in mice. 420 26

Youmans, Guy P. (Northwestern University Medical School, Chicago, Ill.), and Anne S. Youmans. Nonspecific factors in resistance of mice to experimental tuberculosis. J. Bacteriol. 90:1675-1681. 1965.-In contrast to viable attenuated mycobacterial cells, Escherichia coli lipopolysaccharide (LPS) did not produce an acute pulmonary granulomatous response in mice, did not decrease the tolerance of mice to early subsequent intravenous injections of viable attenuated mycobacterial cells, nor did it increase susceptibility to tuberculous infection when injected simultaneously with virulent mycobacterial cells. When the injection of E. coli LPS was followed by the intravenous injection of virulent mycobacterial cells, there was a moderate increase in resistance to tuberculous infection which was maximal 7 to 14 days after the LPS injection. The degree of increased resistance to tuberculous infection was approximately the same as that produced by nearly maximal tolerated doses of heat-killed attenuated mycobacterial cells, and to that produced by a trichloroacetic acid extract of heat-killed attenuated mycobacterial cells. It is suggested that the major, if not entire, immunizing component of heat-killed attenuated mycobacterial cells resides in a heat-stable "nonspecific" component. A "multiple response" theory of immunity to tuberculosis is proposed.
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PMID:Nonspecific factors in resistance of mice to experimental tuberculosis. 495 57

The identity of a heteropolysaccharide from cell walls of Mycobacterium tuberculosis H37Ra with Seibert's tuberculopolysaccharide I was demonstrated by thin-layer chromatography, chemical analysis, and antigenic tests. The polysaccharide of M. kansasii was shown to be identical with that of M. tuberculosis. Defatted cells were disintegrated by ultrasonic treatment in the presence of glass beads; cell walls were obtained by differential ultracentrifugation. Ethyl alcohol-precipitated carbohydrate extracts were analyzed for protein and nucleic acid; these impurities were removed. Tuberculopolysaccharide I from the mycobacterial culture filtrate is probably derived from a lipopolysaccharide of the cell wall, which is partially removed by chloroform in the intact state. Alkaline extraction releases additional polysaccharide, in varying degrees of association with cell wall murein.
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PMID:Chemical and serological relationships between the heteropolysaccharides of Mycobacterium tuberculosis and Mycobacterium kansasii. 496 49

Metritis was elicited by intrauterine infusion of tuberculin or killed Campylobacter fetus ssp. venerealis into vaccinated guinea pigs and lipopolysaccharide or immune complexes into normal animals. The local inflammatory response to intrauterine infusion of antigens, lipopolysaccharide, and immune complexes was determined by changes in differential cell counts in the uterine lavage fluid and by histopathological examination of uterine tissue. The percentage of neutrophils was significantly (p less than 0.01) greater in uterine lavage fluid collected at 4 hr after infusion of tuberculin into animals vaccinated locally (intrauterine) with M. tuberculosis than in animals vaccinated parenterally (subcutaneously). In contrast, the local response to infusion with C. fetus ssp. venerealis was approximately the same in animals vaccinated intrauterine and subcutaneously with Campylobacter. The systemic response, measured by the delayed type hypersensitivity cutaneous reaction to intradermal injection of tuberculin, was significantly (p less than 0.01) greater in animals vaccinated subcutaneously than intrauterine. Similarly, the concentration of Campylobacter antibody in the serum of animals vaccinated subcutaneously was significantly (p less than 0.01) greater than in guinea pigs vaccinated intrauterine. The intrauterine infusion of immune complexes, composed of C. fetus ssp. venerealis and corresponding antibody, into the uterus of normal guinea pigs stimulated neutrophil migration into the uterine lumen. Infusion of lipopolysaccharide also stimulated neutrophil migration into the uterine lumen. A correlation between an increased percentage of neutrophils in uterine lavage fluid and infiltration of the uterine epithelium with neutrophils was observed.
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PMID:Immune-mediated migration of neutrophils into the uterine lumen of guinea pigs. 624 31

Four monocyte functions were studied in patients with pulmonary tuberculosis and in healthy subjects. Circulating monocytes from four of six patients with tuberculosis functioned as suppressor cells; depletion of adherent cells from mononuclear cells obtained from the peripheral blood of these patients resulted in a 37-fold enhancement in tuberculin purified protein derivative-induced incorporation of [3H]thymidine. Monocytes from patients with tuberculosis exhibited increased adherence to plastic. Plasma from patients with tuberculosis also increased the adherence of monocytes from healthy subjects. However, basal and lipopolysaccharide-stimulated production of prostaglandin E2 by monocytes and tumoricidal activity were not altered in patients with tuberculosis. Thus, tuberculosis in humans is associated with the enhancement of selective monocyte functions. The dissociation in monocyte effector functions in human mycobacterial infection has potential implications not only for the course of tuberculosis but also for immunoadjuvant therapy.
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PMID:Augmentation of selective monocyte functions in tuberculosis. 694 16

Previous studies have demonstrated that, like bacterial lipopolysaccharide (LPS), arabinofuranosyl-terminated lipoarabinomannan (AraLAM) from an attenuated strain of Mycobacterium induces potent early gene (c-fos, KC, JE and TNF-alpha) responses in murine macrophages, whereas extensively alpha-Manp capped LAM (ManLAM) from virulent M. tuberculosis do not. In this study we have extended analysis of the influence of mycobacterial LAM on macrophage function by demonstrating that AraLAM (but not ManLAM), like bacterial LPS, is a potent stimulator of inducible nitric oxide synthase (iNOS) expression independent of the autocrine activity of co-stimulated tumour necrosis factor-alpha (TNF-alpha) release. The inability of ManLAM to induce iNOS expression was not due to induction of the 'deactivating' cytokine interleukin-10 (IL-10). Indeed, like LPS, AraLAM was also a potent inducer of IL-10 expression. However, analysis of AraLAM- or LPS-induced responses in the presence of interferon-gamma (IFN-gamma) showed that, whereas IFN-gamma acts as a potent co-stimulus for iNOS, it completely inhibits the IL-10 response. Hence, the presence of IFN-gamma early in infection will have an important immunomodulatory role in determining the macrophage response. These results have important implications for the pathogenesis of virulent and avirulent mycobacteria in vivo.
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PMID:Opposing effects of interferon-gamma on iNOS and interleukin-10 expression in lipopolysaccharide- and mycobacterial lipoarabinomannan-stimulated macrophages. 754 44

In a number of mammalian cell types, pteridine biosynthesis from guanosine 5'-triphosphate and formation of nitric oxide from L-arginine are induced by gamma interferon (IFN-gamma) and bacterial lipopolysaccharide (LPS). We assessed the possibility of using such metabolic alterations for the in vitro detection of pyrogens. Products from gram-negative and gram-positive bacteria and related synthetic compounds were tested for their potential to induce either of these pathways. Stimulation of pteridine biosynthesis was monitored as the formation of neopterin in the human myelomonocytic cell line THP-1. The formation of nitric oxide was determined as nitrite in murine J774A.1 macrophage cultures. The substances tested included toxic and detoxified parts of LPS and lipid A from Escherichia coli, Salmonella typhimurium, Salmonella minnesota, and Klebsiella pneumoniae as well as lipoteichoic acid and toxic shock syndrome toxin 1 from Staphylococcus aureus. Furthermore, two cell wall compounds from Mycobacterium tuberculosis, trehalose 6,6'-dimycolate and N-acetylmuramyl-L-alanyl-D-isoglutamine, which are active components of Freund's adjuvant, were used. When applied as a single stimulus, only the whole LPS molecule potently stimulated neopterin or nitrite formation. Lipid A and products from gram-positive bacteria were weakly active. For neopterin formation, lipid A required the presence of fetal calf serum. Besides detoxified LPS and independently from the presence of serum, all bacterial compounds tested strongly increased the effects mediated by IFN-gamma. Our results show that bacterial pyrogens can be detected by monitoring the formation of neopterin or nitrite. This may provide a basis for the development of an in vitro assay for the detection of pyrogenic contamination with the aim of replacing the currently used animal test.
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PMID:Detection of bacterial pyrogens on the basis of their effects on gamma interferon-mediated formation of neopterin or nitrite in cultured monocyte cell lines. 766 77

M. tuberculosis, the aetiological agent of tuberculosis readily infects and multiplies within the macrophages of the host. Macrophage activation is known to occur through a series of stages, which results in the production of biologically active molecules such as the reactive oxygen and nitrogen intermediates. The following study was conducted on 20 patients with pulmonary tuberculosis, before and after initiation of antituberculous therapy, and on 10 normal healthy controls. The macrophages were isolated from peripheral blood of the patients and controls at a concentration of 1 x 10(6) cells ml-1. The generation of reactive oxygen intermediates was measured by a chemiluminescence technique. Reactive nitrogen intermediates, were measured following stimulation of macrophages with latex, lipopolysaccharide (LPS) and purified protein derivative-S (PPD-S). Citrulline levels and electron transport chain activity were also determined in the cell cultures. It was observed that there was a significant depression (p < 0.05) in the respiratory burst response in the patient group (0.46 x 10(3) +/- 0.11 cpm per 10(6) cells) compared with the controls (7.12 x 10(3) +/- 2.31 cpm per 10(6) cells). On the other hand, reactive nitrogen intermediates (671.03 +/- 2.18 nmol) and citrulline levels (193.07 +/- 2.38 nmol) were significantly (p < 0.001) higher before initiation of therapy compared with control values (24.36 +/- 2.81 and 18.91 +/- 2.12 nmol respectively). Their levels declined, during the post-therapy period of 3 months, to 60.81 +/- 2.03 and 38.17 +/- 2.13 nmol respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Release of reactive oxygen and nitrogen intermediates from monocytes of patients with pulmonary tuberculosis. 766 9

The cytokines interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF-alpha) are released by mononuclear phagocytes in vitro after stimulation with mycobacteria and are considered to mediate pathophysiologic events, including granuloma formation and systemic symptoms. We demonstrated that the Mycobacterium tuberculosis cell wall component lipoarabinomannan (LAM) is a very potent inducer of IL-1 beta gene expression in human monocytes and investigated the mechanism of this effect. We localized the LAM-, lipopolysaccharide (LPS)-, and TNF-alpha-inducible promoter activity to a -131/+15 (positions -131 to +15) DNA fragment of the IL-1 beta gene by deletion analysis and chloramphenicol acetyltransferase assay. Within this DNA fragment, there were two novel 9-bp motifs (-90/-82 and -40/-32) with high homology to the nuclear factor-IL6 (NF-IL6) binding site. Site-directed mutagenesis demonstrated that the two NF-IL-6 motifs could be independently activated by LAM, LPS, or TNF-alpha and that they acted in an orientation-independent manner. DNA mobility shift assay revealed specific binding of nuclear protein(s) from LAM-, LPS-, or TNF-alpha-stimulated THP-1 cells to the NF-IL6 motifs. We conclude that the two NF-IL6 sites mediate induction of IL-1 beta in response to the stimuli LAM, LPS, and TNF-alpha.
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PMID:Regulation of the interleukin-1 beta (IL-1 beta) gene by mycobacterial components and lipopolysaccharide is mediated by two nuclear factor-IL6 motifs. 768 3


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