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)

Pasteurella haemolytica is represented by two biotypes (A and T), 15 serotypes, and numerous untypable strains. Specific biotypes and serotypes are associated with fibrinous pleuropneumonia (pneumonic pasteurellosis) in cattle, sheep, and goats, septicemic pasteurellosis in lambs, and mastitis in ewes. Four virulence factors have been associated with P. haemolytica: fimbriae, a polysaccharide capsule, endotoxin [lipopolysaccharide (LPS)], and leukotoxin (LKT). The interactions of these virulence factors with components of the pulmonary alveolus are discussed as a model for the pathogenesis of pasteurellosis. Fimbriae on P. haemolytica may enhance colonization of the upper respiratory tract. The capsule of P. haemolytica varies in composition among serotypes. It inhibits complement-mediated serum killing as well as phagocytosis and intracellular killing of P. haemolytica. The capsule enhances neutrophil directed migration and adhesion of P. haemolytica to alveolar epithelium. Pasteurella haemolytica LPS can alter bovine leukocyte functions, by dose-dependent inhibition or augmentation; it is directly toxic to bovine endothelium; it modifies cardiopulmonary hemodynamics; and it elevates circulatory prostanoids, serotonin, cAMP, and cGMP. Leukotoxin is produced by all known serotypes and many untypable strains. Leukotoxin is a poreforming cytolysin that affects ruminant leukocytes and platelets by altering function at low levels but causing lysis at high levels.
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PMID:Molecular aspects of virulence of Pasteurella haemolytica. 197 1

The in vitro growth of tumor cells infected with mycoplasmas was suppressed by macrophages pretreated with interferon (IFN), but the growth of mycoplasma-free tumor cells was not suppressed. Pretreatment of macrophages with IFN plus mycoplasmas or their soluble factors either simultaneously or sequentially, IFN first and mycoplasmas second, but not in the reverse order, was effective in activating macrophages to suppress the growth of mycoplasma-free tumor cells. Macrophages from C3H/HeJ mice (which respond only slightly to lipopolysaccharide) were activated by IFN plus mycoplasmas or their soluble factor, and their action was not influenced by the addition of a lipopolysaccharide-neutralizing agent, polymyxin B. These results suggest that the macrophage-activating agent in mycoplasmas does not mimic lipopolysaccharide. The administration of mycoplasmas plus IFN to mice with ascitic or solid tumors resulted in the reduction of tumor growth. The survival rate of tumor-bearing mice was improved by the administration of mycoplasmas, and this was synergistically enhanced by the addition of IFN. These results indicate (a) that mycoplasmas can be useful as a biological response modifier, and (b) that care should be taken to prevent contamination with mycoplasmas in experiments on macrophage activation.
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PMID:Induction of antitumor activity in macrophages by mycoplasmas in concert with interferon. 212 81

Five cesarean-derived, colostrum-deprived pigs were given three adjuvant-supplemented subcutaneous and one intravenous injection of the purified 104-kDa hemolysin from serotype 1 Actinobacillus pleuropneumoniae CM-5. Six control animals received phosphate-buffered saline only. Five of six control pigs died within 24 h after challenge. The sixth control pig was moribund and euthanized after 48 h. All six pigs had pleuropneumonia, and A. pleuropneumoniae was isolated from all six lungs. None of the vaccinated pigs died as a result of challenge. After being euthanized, two pigs in this group had no lung lesions but three had chronic pleuropneumonia involving 10, 20, and 40% of the lung tissue. A. pleuropneumoniae was isolated from lung lesions of these three animals but not from the two pigs without lesions. The prechallenge hemolysin-neutralizing antibody titers in the vaccinated pigs were 1:10,900, 1:10,600, 1:4,800, 1:3,900, and 1:3,000, in order of increasing lung involvement. None of the control pigs had neutralizing antibodies. Enzyme-linked immunosorbent assay (ELISA) antibodies to capsule, lipopolysaccharide, and hemolysin were not detected in serum samples collected from the control pigs. In the vaccinated group, prechallenge sera did not contain ELISA antibodies to capsule or lipopolysaccharide. ELISA antibodies to the hemolysin were detected only in the prechallenge and postchallenge serum samples. These results indicate that pigs immunized with the 104-kDa hemolysin of serotype 1 A. pleuropneumoniae are protected against challenge with virulent bacteria. The association between neutralizing antibodies and protection indicates indirectly that the hemolysin is an important virulence factor.
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PMID:Humoral antibody response and protective immunity in swine following immunization with the 104-kilodalton hemolysin of Actinobacillus pleuropneumoniae. 225 12

Heat-inactivated (60 degrees C, 45 min) Mycoplasma capricolum strain JR cells activate murine macrophages to secrete high levels of tumor necrosis factor alpha (TNF alpha) and to lyse tumor target cells efficiently. Fractionation of the intact M. capricolum cells, obtained from cells harvested at the exponential phase of growth, shows that their capacity to induce TNF alpha secretion by macrophage resides exclusively in the membrane fraction. The macrophage-mediated cytolysis following activation by M. capricolum membranes was significantly inhibited by specific anti-recombinant murine TNF alpha antibodies. M. capricolum membranes are a potent inducer of TNF alpha as the commonly used bacterial lipopolysaccharide, indicated by their dose-response curve for macrophage activation. Our study further showed that M. capricolum membranes and lipopolysaccharide synergize to augment TNF alpha secretion by C57BL/6-derived macrophages markedly. Moreover, lipopolysaccharide-unresponsive C3H/HeJ-derived macrophages, were pronouncedly activated by M. capricolum membranes, which do not contain lipopolysaccharide. These findings suggest that the mechanism by which M. capricolum membranes activate macrophages differs from that of lipopolysaccharide. Results of preliminary experiments show that human monocytes as well secrete TNF alpha following activation by M. capricolum membranes. Thus, in contrast with the prohibitive toxicity of lipopolysaccharide to animals and humans, M. capricolum membranes, which contain no lipopolysaccharide and are nontoxic in nature, may be of therapeutic value in the treatment of cancer.
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PMID:Mycoplasma capricolum membranes induce tumor necrosis factor alpha by a mechanism different from that of lipopolysaccharide. 232 37

Pleuropneumonia is an important disease of swine caused by Actinobacillus pleuropneumoniae. Putative virulence determinants include capsule, lipopolysaccharide, and cytotoxin. We studied the virulence and virulence determinants of 2 strains: CM5 and CM5A of serotype 1. Strain CM5 was isolated from a pig with pleuropneumonia and passaged once in vitro; strain CM5A was a substrain of CM5 passaged 70 times in vitro. Pigs challenge exposed to an aerosol of 1.3 x 10(7) colony-forming units of CM5/ml died within 30 hours; pigs challenge exposed to an aerosol of 1.6 x 10(8) colony-forming units of CM5A/ml survived. The average thickness of the capsular layer was 137 nm in strain CM5 and 53 nm in strain CM5A in bacteria treated with homologous antibody and examined by transmission electron microscopy. Similarly, capsular material binding polycationic ferritin was found in colonies of strain CM5, but not in strain CM5A. The ratio of hexosamine to protein in extracted capsule of CM5 was more than twice that of CM5A. The polyacrylamide gel electrophoretic profile of the lipopolysaccharide, outer membrane proteins, and whole cell proteins did not differ between the 2 strains. Also, the amount of cytotoxin or endotoxin produced by the 2 strains during the logarithmic growth phase was not different. The electrophoretic profile of restriction endonuclease digested DNA was similar, with the exception of bands in the 750- and 620-basepair regions. It was concluded that attenuation of strain CM5A during in vitro passage was a result of reduced capsule production and that encapsulation is an important virulence determinant of A pleuropneumoniae, serotype 1.
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PMID:Characterization of an attenuated strain of Actinobacillus pleuropneumoniae, serotype 1. 233 67

The role of the monocyte in human cytomegalovirus (HCMV)-induced immunosuppression was examined by assessing the ability of the virus to directly suppress various monocyte accessory cell functions. Both patient-derived and laboratory-adapted strains of HCMV were capable of impairing antigen-presenting functions of purified human monocytes. In seven of 12 virus-infected samples, there was a significant decrease (P less than 0.05) in the ability of HCMV-infected monocytes to present tetanus toxoid to autologous lymphocytes compared with mock-infected controls; similar results were obtained with Candida albicans and mumps. In contrast, the response to PHA was impaired in only one of eight HCMV-infected samples. The increased expression of MHC class II Ia antigens (HLA-DQ and HLA-DR) by monocytes after stimulation by interferon-gamma was impaired in approximately one-third of the 43 virus-infected samples tested. Interleukin-1 (IL-1) production after incubation with the stimulating antigens, however, was unaffected. Attempts to augment immuno-suppression by co-stimulation of monocytes with lipopolysaccharide (LPS), heat-killed Escherichia coli or Listeria monocytogenes were not successful; however, dramatically increased levels of immunosuppression was obtained with HCMV preparations containing mycoplasma. Thus, although HCMV is capable of directly perturbing monocyte accessory cell functions, the variability and partial suppression observed suggests that infection of monocytes by HCMV alone is not sufficient to produce the levels of immune hyporesponsiveness observed in HCMV-infected patients.
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PMID:Suppression of monocyte functions by human cytomegalovirus. 253 90

We and other investigators have previously demonstrated that mycoplasmas induce macrophage-mediated lysis of tumor cells, but the mechanism responsible for this process had, thus far, not been clarified. We now report that addition of either viable or heat-killed Mycoplasma orale to murine macrophages induces a cytolytic activity which, due to its neutralization by a specific antiserum against murine cloned recombinant tumor necrosis factor (rTNF), was identified as TNF-mediated. Both thioglycollate-elicited peritoneal macrophages and the normal macrophages cloned from our JBM phi 1.1 bone-marrow-derived cell line effectively produced TNF at levels similar to, or higher than, those obtained in the presence of high concentrations of lipopolysaccharide (LPS). Four other mycoplasma species demonstrated a varied capacity to induce TNF production by macrophages. Elevated TNF levels were also observed during macrophage-mediated cytolysis of murine A9 fibrosarcoma cells in the presence of either M. orale or LPS. Addition of the specific antiserum against rTNF at a concentration which neutralized all TNF activity in the co-cultures partially inhibited concomitant A9 cell killing. We can, therefore, conclude that M. orale induces TNF production which is, at least partially, responsible for subsequent tumor cell killing.
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PMID:Tumor necrosis factor as a mediator of Mycoplasma orale-induced tumor cell lysis by macrophages. 272 Jul 90

During the screening of suppressor T cell (Ts) hybridomas for antigen-nonspecific suppressive activity, we isolated a strain of Mycoplasma arginini which inhibits B cell antibody production in vitro. The addition of mycoplasma-containing Ts hybridoma culture supernatant to splenic B cells responding to sheep red blood cells (SRBC) and T cell-replacing factor or to trinitrophenyl-lipopolysaccharide (TNP-LPS) suppressed the production of anti-SRBC and anti-TNP plaque-forming cells in a dose-dependent and antigen-nonspecific manner. Inhibition occurred due to the noncytotoxic mycoplasmal infection of B cells in culture and required the physical presence of microorganisms. Cell cycle analysis of acridine orange-stained B cells indicated that mycoplasmal infection did not block cell cycle entry and progression of antigen-activated cells. In addition to a suppressive activity, this strain of mycoplasma was selectively mitogenic for B cells. Furthermore, the mycoplasma failed to stimulate or inhibit T cell proliferation. The suppressive and mitogenic activities were selectively absorbed by mitogen-activated B cells but not T cells. These results indicate that this strain of M. arginini mimics the suppressive activity of an antigen-nonspecific Ts factor selective for B cell antibody production.
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PMID:The regulation of murine B cell differentiation. I. Nonspecific suppression caused by Mycoplasma arginini. 279 Sep 65

Culture supernatant from a human T-cell leukemia virus type I (HTLV-1)-infected cell line, DGA-1, contained a novel macrophage-activating factor (MAF). This MAF was antigenically and functionally distinct from interferon-gamma (IFN-gamma) and from granulocyte-monocyte colony-stimulating factor (GMCSF). Potential contaminants such as bacterial lipopolysaccharide (LPS), Mycoplasma spp, and HTLV-1 were not responsible for this MAF activity. The DGA-1 MAF was secreted constitutively and the cell line grew well in the absence of growth factors such as interleukin-2, mitogen, or antigen. This cell line should provide a good source of this MAF for further purification and characterization.
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PMID:A novel human macrophage-activating factor: distinction from interferon-gamma (IFN-gamma) and granulocyte-macrophage colony-stimulating factor (GMCSF). 283 73

A class of interleukin-2-dependent T-cell clones, isolated from a murine fetal thymus, was previously shown to suppress the induction of cytotoxic responses to alloantigens (H.-S. Teh, M. Ho, and W. R. McMaster, J. Immunol. 135:1582-1588, 1985). In that article, the immunosuppressive properties of these T-cell clones were shown to be a direct consequence of infection by Mycoplasma hyorhinis. Suppression of cytotoxic responses was mediated by both the mycoplasmas and a 200-kilodalton factor present in supernatants of infected cultures. This factor was sensitive to proteases but was resistant to heating to 60 degrees C for 1 h and to incubation on ice at pH 2 or pH 14 for 4 h. The production of suppressor factor in infected cultures was independent of the viability or the protein synthesis capability of the mammalian cells, suggesting that it was produced by M. hyorhinis. The factor was most suppressive when it was added during the early stages of the cytotoxic response. Its suppressive effects on cytotoxic responses were not reversed by the addition of an excess of recombinant interleukin-2. This factor also suppressed mitogenic responses to lipopolysaccharide. However, it is not a growth inhibitor since it did not affect the proliferation of tumor cell lines. A simple method for detecting M. hyorhinis in the infected T-cell clones and for eliminating it is described.
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PMID:Suppression of cytotoxic responses by a supernatant factor derived from Mycoplasma hyorhinis-infected mammalian cell lines. 325 4


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