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

In this communication we discuss preliminary evidence suggesting a very strong synergism between tumour necrosis factor (TNF) and lipopolysaccharide (LPS) or between TNF and other bacteria in causing haemorrhagic necrosis and lethal shock. We found that TNF by itself does not cause haemorrhagic necrosis when injected into normal skin. TNF also had a rather low systemic toxicity when injected into disease-free, germfree-derived, defined-flora animals. On the other hand the addition of small amounts of LPS markedly raised the lethality of intravenous TNF treatments, and LPS injected into normal skin 'prepared' the site of injection for subsequent induction of haemorrhagic necrosis by locally injected TNF. Similar synergism was observed between TNF and mycoplasma. We suggest that the synergism between TNF and bacterial endotoxin (or other bacteria or bacterial products) may be part of an important defence mechanism against infections which is independent of specific immunity mediated by B and T cells. This synergism may be useful in increasing the therapeutic effects of TNF on tumours if the development of systemic toxicity in this treatment can be prevented.
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PMID:Relationship of tumour necrosis factor and endotoxin to macrophage cytotoxicity, haemorrhagic necrosis and lethal shock. 333 8

We find a strong synergism between tumor necrosis factor (TNF) and bacteria or their products. Endotoxin-"free" recombinant TNF, even at very high doses (160 micrograms), did not alone cause hemorrhagic necrosis (HN) in the skin of normal mice. Similarly, TNF alone had a low systemic toxicity in tumor- and pathogen-free mice. However, TNF given intravenously with nanogram quantities of the endotoxin lipopolysaccharide caused lethal shock. Furthermore, subcutaneous injection of lipopolysaccharide made skin susceptible to subsequent induction of HN by TNF injected in the same site 24 hr later. Mycoplasma-infected cells or corynebacteria also synergized with TNF to cause HN or lethal shock. In addition, we find that lymphotoxin, a cytokine functionally and genetically related to TNF, also synergized with the bacteria to cause HN, whereas interleukin 1 alpha or interferon gamma did not. Together, the results indicate that a synergy between TNF and bacteria or their products causes HN and lethal shock in normal mice.
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PMID:Synergy between tumor necrosis factor and bacterial products causes hemorrhagic necrosis and lethal shock in normal mice. 342 44

B lymphocytes, preactivated by lipopolysaccharide (LPS), could be triggered to growth by a strain of Mycoplasma arginini, while the level of immunoglobulin (Ig) secretion, quantitated as the number of plaque-forming cells (PFC), was low. The PFC response could be increased by the addition of conditioned media (CM) from lectin-activated spleen cells or T cell tumour EL-4 to the culture of preactivated B cells. CM did not by itself induce a significant amount of PFC in the cultures of LPS-preactivated B cells. The maturation enhancing activity was distinct from IL-2 and B cell growth factor as judged by gel exclusion chromatography.
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PMID:Enhancement of immunoglobulin secretion by the lymphokine-like activity of a Mycoplasma arginini strain. 348 65

Intact Haemophilus pleuropneumoniae cells (strain Shope 1, serotype 1), highly purified lipopolysaccharide (LPS) obtained from this strain of H pleuropneumoniae, as well as from Escherichia coli O111:B4, filter-sterilized H pleuropneumoniae cell-free culture supernatant fluid, and heat-inactivated supernatant fluid were given intranasally to CF1 mice and intratracheally to pigs. Pulmonary lesions induced by H pleuropneumoniae in mice were similar to those induced by H pleuropneumoniae in pigs. Histologically, lungs of mice and pigs killed 1 or 2 days after inoculation with 200 micrograms of highly purified H pleuropneumoniae LPS had lesions similar to one another and were similar to those in mice and pigs given intact H pleuropneumoniae, except that little or no necrosis or hemorrhage was observed. In mice killed 1 or 2 days after inoculation of 200 micrograms of E coli O111:B4 LPS, pulmonary lesions were similar to those in mice given H pleuropneumoniae LPS. Pulmonary lesions in mice given cell-free culture supernatant fluid obtained from a midlog-phase growth culture of H pleuropneumoniae cultivated in a chemically defined medium were severe and consisted of neutrophil infiltration and extensive necrosis. In mice, the heat-inactivated supernatant fluid produced mild lesions that consisted of foci of neutrophil aggregation and no necrosis. Extensive necrosis observed in lesions caused by cell-free culture supernatant fluid could be attributed to the action of a heat-labile component, perhaps by the extracellular heat-labile hemolysin produced by H pleuropneumoniae cultivated in chemically defined medium. A LPS endotoxin and a heat-labile factor may be involved in the pulmonary lesion development in the acute phase of porcine Haemophilus pleuropneumonia.
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PMID:Role of haemophilus pleuropneumoniae lipopolysaccharide endotoxin in the pathogenesis of porcine Haemophilus pleuropneumonia. 359 76

Oligosaccharides of smooth-type lipopolysaccharide (LPS) and oligosaccharides of rough-type LPS were isolated from Haemophilus pleuropneumoniae and conjugated to tetanus toxoid by reductive amination. The antigenic and immunogenic characteristics of the oligosaccharides, the oligosaccharide-tetanus toxoid conjugates, and the LPS of H. pleuropneumoniae were determined by passive hemagglutination, enzyme-linked immunosorbent assay, and inhibition enzyme-linked immunosorbent assay with antisera produced by immunization of rabbits and pigs. The findings were compared with the immunologic response induced by immunization of pigs with an H. pleuropneumoniae whole-cell vaccine and by infection of pigs with viable H. pleuropneumoniae. The results show that conjugation of isolated oligosaccharides of H. pleuropneumoniae to tetanus toxoid improves the immunogenicity of the oligosaccharides without significantly altering their antigenic character. These findings extend the understanding of the immunobiology of H. pleuropneumoniae infection in pigs and suggest the potential of purified oligosaccharides as vaccines to prevent porcine pleuropneumonia.
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PMID:Vaccine potential of Haemophilus pleuropneumoniae oligosaccharide-tetanus toxoid conjugates. 377 Sep 54

Cells from the murine B lymphoma I.29, expressing IgM or IgA of identical idiotype, were found inducible by lipopolysaccharide to differentiate into plasma cells. Within 3 days, differentiating cells lost membrane-bound immunoglobulin (Ig) and accumulated large quantities of intracytoplasmic Ig. At day 6 of culture, IgA secretion increased 50-100-fold, as determined by enzyme-linked immunoassay. Proliferation increased for the first days of culture but decreased thereafter; by day 10 very few viable cells were present in lipopolysaccharide-stimulated cultures. Similar results were obtained by culturing I.29 cells in the presence of supernatants of certain B cell lines (e.g. BFO.3). The finding of a strict correlation between the inductive activity and presence of contaminating Mycoplasma fermentans suggested that factor(s) released by mycoplasma were responsible for the mitogenic activities. This was further indicated by the findings that: the supernatants of BFO.3 that were rendered free of mycoplasma were not inductive, and a nonactive cell line could be made active by infection with supernatants of BFO.3 cells containing viable microorganisms. Thus, supernatants of mycoplasma-infected cell lines may act as potent polyclonal activators on both normal and malignant B lymphocytes. The ability to induce membrane Ig on 70Z/3 cells indicates that mycoplasma-related mitogens are also active on pre-B cells. The possibility of mycoplasma contamination should thus be carefully excluded when presumptive factors of cloned cell lines are being evaluated.
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PMID:Differentiation in the murine B cell lymphoma I.29: inductive capacities of lipopolysaccharide and Mycoplasma fermentans products. 387 69

Mycoplasma orale, maintained as a contaminant of a mouse hybrid cell line, induces an intense proliferation in short-term culture of lymphoid cells of inbred mice. Cell division induced by the contaminated cell culture fluid reaches a maximum on day four and declines rapidly thereafter. Culture fluids from hybrid cells freed of contamination do not cause proliferation. Cells from the spleen, bone marrow, and thymus of each of several strains of inbred mice, including xid CBA/N, poorly responsive to lipopolysaccharide, are stimulated by the mitogen, as are cells from BALB/c nude mice. The characteristics of the stimulatory effect are analogous in several important aspects to those of naturally occurring T cell-derived growth factors. In the absence of detectable numbers of T cells, both small and large B lymphocytes undergo mitosis in the presence of contaminated cell culture fluid, and B cells stimulated to divide by lipopolysaccharide are sustained for further rounds of replication by M. orale-containing cell culture fluid. The fluid also augments the stimulatory effect on thymocytes of suboptimum concentrations of phytohemagglutinin mimicking the effect of interleukin-1. Unlike with most naturally occurring lymphoid cell mitogens, however, the dividing cells do not go on to immunoglobulin secretion.
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PMID:Stimulation of lymphoid cell proliferation by Mycoplasma orale, a common cell culture contaminant. 387 89

Culture fluid (CF) from LA cells (LA-CF) strongly stimulated the proliferation of normal A/J mouse spleen cells in vitro. This activity was nondialyzable, labile to 56 degrees C for 20 min., sedimentable, H-2 and species unrestricted, and was found to be mycoplasma-derived. LA-CF was active for B cells because in vitro treatment of A/J spleen cells with anti mouse Ig antiserum and complement eliminated their responsiveness to LA-CF. LA-CF stimulated the resting, small spleen cells of the nude mouse as strongly as lipopolysaccharide (LPS) did. Spleen cells of the X chromosome-linked immunodeficiency (Xid) mouse were stimulated by LPS to a half of the control mice, and by LA-CF to a quarter of the control. LPS-low responder (C3H/HeJ) spleen cells were also stimulated by LA-CF. The mycoplasma(s)-derived B cell mitogen in the LA-CF was different from LPS.
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PMID:Comparison of mycoplasma(s)-derived B cell mitogenic activity with lipopolysaccharide. 390 4

Immunohistochemical, enzyme-histochemical and electron-microscopical methods were used to study non-lymphoid cells of control and stimulated rat bronchus associated lymphoid tissue (BALT) in situ and in suspensions. Particular attention was paid to the so-called antigen-handling cells, i.e., the interdigitating cells (IDC), which are situated in the T-cell areas, the follicular dendritic cells (FDC), which appear to be restricted to germinal centers, and macrophages, present both in T-cell and B-cell areas. The interdigitating cells were distinguished by being Ia-positive and by the presence of acid phosphatase and non-specific esterase activity in an area near the nucleus. Follicular dendritic cells could be observed in situ by using a monoclonal antibody and by the in vitro trapping of HRP-anti-HRP complexes. Several types of macrophages were found. At the electron-microscopical level no well-developed IDC and FDC could be detected in control BALT. However, in BALT of lipopolysaccharide-stimulated and mycoplasma-infected rats, well-developed IDC and FDC were found. It can be concluded that IDC's and FDC's can be found in BALT.
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PMID:Non-lymphoid cells of bronchus-associated lymphoid tissue of the rat in situ and in suspension. With special reference to interdigitating and follicular dendritic cells. 396 78

The lipids and lipopolysaccharides of five mycoplasmas were examined for complement-fixing activity to antimembrane rabbit sera. Total glycolipid fractions and the aqueous phenol fractions (lipopolysaccharides) from the membranes of Acholeplasma laidlawii, A. modicum, A. axanthum, and Mycoplasma neurolyticum exhibited significant antigenic activity. The glycolipids and phosphoglycolipids from Thermoplasma acidophilum were either anticomplementary or did not react due to their extreme hydrophobic nature. High activity was found using the lipopolysaccharide of T. acidophilum. The pure glycolipids and phosphoglycolipids of the Acholeplasma and Mycoplasma species also exhibited significant complement-fixing activity. Acylation of the sugar residues of these lipids reduced or negated complement-fixing activity. Double cross-reactions between the glycolipids of A. laidlawii and A. modicum appeared to be due to mono- and diglucosyl diglycerides of identical structure. Specificity of glycolipid structure was noted by the absence of cross-reactions between A. laidlawii and M. neurolyticum, the glycolipids of which differ only in the nature of the glucose linkages. The existence of lipopolysaccharides in the membranes of mycoplasmas and their complement-fixing activity in the presence of antimembrane sera suggest their possible importance as specific antigenic determinants.
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PMID:Immunological analysis of glycolipids and lipopolysaccharides derived from various mycoplasmas. 421 61


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