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)

We have performed experiments designed to evaluate the potential contribution of endotoxin contamination to lymphocyte reponses. Saline and EDTA extracts of 4 different strains of gram negative bacteria were examined for their capacity to initiate mitogenic responses in murine spleen cells. As compared to phenol extracts of these bacteria which contain primarily lipopolysaccharide-LPS, these saline and EDTA extracts were significantly less active in this assay. The mitogenic activity which was present was also manifest in spleen cells from the C3H/HeJ mouse, whereas phenol-extracted LPS preparations were inactive. In addition, mitogenic activity of saline and EDTA extracts was not blocked by polymyxin B, an agent known to abrogate LPS mediated responses. We conclude that LPS contamination may not normally be as significant a problem as had earlier been assumed. However, when endotoxin contamination is present, neither the use of C3H/HeJ spleen cells nor polymyxin B is an appropriate test to evaluate this possibility.
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PMID:The use of polymyxin B and C3H/HeJ mouse spleen cells as criteria for endotoxin contamination. 22 47

Endotoxin was shown to depress neutrophil bactericidal activity while enhancing Nitro Blue Tetrazolium reduction and hexose monophosphate shunt activity. Separation of bactericidal action from oxidative metabolism suggests that the effect of endotoxin might involve the formation of reactive oxygen radicals such as superoxide. Chemiluminescence often accompanies metabolic activation of polymorphonuclear neutrophils (PMNs). However, human PMNs did not show chemiluminescence when challenged with endotoxin (lipopolysaccharide; LPS) or lipid A. Superoxide formation was also unaffected by endotoxin. In contrast, preincubation of PMNs with LPS for 30 min produced significant depression of chemiluminescence, oxygen consumption, and superoxide formation. Decreased chemiluminescence was not the result of complement consumption. In a cell-free system, superoxide was not scavenged by LPS, nor did LPS stimulate superoxide dismutase. Oxidase enzymes for reduced nicotinamide adenine dinucleotide or reduced nicotinamide adenine dinucleotide phosphate harvested from broken cells were not affected by LPS. The toxicity of LPS may reside in its ability to activate the PMNs while simultaneously blocking bactericidal capacity.
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PMID:Endotoxin in vitro interactions with human neutrophils: depression of chemiluminescence, oxygen consumption, superoxide production, and killing. 22 88

This is the first report describing in vivo biologic activities elicited by a non-toxic, polysaccharide-rich, water soluble fraction obtained by partial acidic hydrolysis from endotoxic lipopolysaccharide. The two activities present in this preparation were a) mouse bone marrow cell colony formation stimulation (CSF) and b) protection of mice against lethal irradiation. With polysaccharide-deficient rough mutants of salmonella minnesota, the CSF-inducing activity could be restricted to the "core" region of the LPS structure. Sixty-minute hydrolysis with 1 N HCl at 100 degrees C or 0.1 M sodium metaperiodate oxidation at cold room temperature completely abolished CSF-inducing activity of the preparation, whereas it showed considerable resistance to mild alkaline hydrolysis. These findings indicate that the active component in this preparation is carbohydrate in nature. Lipid preparations from smooth LPS or from Re rough mutants are either much less active or completely inactive in the above two assays. The fully active polysaccharide rich preparation was found to be inert in seven other characteristic endotoxicity parameters.
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PMID:Relation of structure to function in bacterial endotoxins. VIII. Biological activities in a polysaccharide-rich fraction. 23 55

Endotoxin (lipopolysaccharide, LPS) treated with ferric chloride was tested for its potential as a non-toxic agent for enhancement of non-specific host resistance. A 1 mg dose of untreated endotoxin, injected i.p. into mice, resulted in 100 per cent mortality, whereas the same amount of chemically-treated endotoxin resulted in less than 35 per cent lethality. The radio-protective potential of the treated endotoxin was similar to that of untreated endotoxin, as 70 per cent of each group of mice tested with either substance survived a dose of 850 rad x-ray. Irradiated mice, challenged 8 days after 850 rad x-irradiation, died when injected with 25 mug of either untreated or treated endotoxin. Antibiotic decontamination of the intestinal tract of host animals reduced the possibility of toxicity from endogenous endotoxin after challenge. This treatment resulted in 100 per cent survival from a 25 mug challenge at 8 days post-irradiation. The ferric chloride-treated proved to be a more effective B-lymphocyte mitogen. At a dose of 100 mug, treated endotoxin resulted in a 50 per cent greater mitogenic stimulation of B-lymphocytes as compared with that found after exposure to untreated endotoxin. Several lines of evidence support the contention that tolerance to untreated endotoxin was induced by repeated injections of either endotoxin preparation 1) 100 per cent of all endotoxin-tolerant mice survived a 1 mg challenge dose of untreated endotoxin, 2) there was a reduced mitotic response of splenic B-lymphocytes after re-exposure with untreated endotoxin as compared with that observed for cells derived from saline-treated mice, and 3) all antibiotic decontaminated mice engrafted with spleen cells from mice made tolerant to either endotoxin preparation survive graft-versus-host disease. In conclusion, based on survival data from normal mice, ferric chloride-treated endotoxin is safer to use than normal endotoxin. Also, treated endotoxin can elicit biologic responses similar in magnitude to those found after injection of mice with untreated endotoxin.
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PMID:Evaluation of biologic activity of ferric chloride-treated endotoxin in mice. 23 54

B cells from CBA/N mice did not form colonies in semisolid agar cultures under circumstances where normal B-cell clonal proliferation is linear with respect to the number of functional cells cultured. This was no due to the unresponsiveness of CBA/N cells to mitogens, and under appropriate liquid culture conditions many CBA/N lymphocytes differentiated to plasma cells containing large amounts of IgM in response to LPS. On the other hand, the same cells proliferated and matured poorly in liquid cultures prepared at low-cell density. The frequency of granulocyte-macrophage progenitors and multipotential hemopoietic stem cells in bone marrow, ability of peritoneal macrophages to elaborate soluble enhancing factors, and levels of serum inhibitors were normal in CBA/N mice. Together with the results of cell-mixing experiments, these findings confirm the selective and intrinsic nature of the CBA/N deficiency. It is suggested that the B-cell cloning technique may be of value in selectively enumerating and assessing functional capability of thymus-independent B cells. C3H/HeJ mice which have previously only been known to be hyporesponsive to certain forms of lipopolysaccharide had a subnormal incidence of colony-forming B cells.
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PMID:Defective colony formation by B lymphocytes from CBA/N and C3H/HeJ mice. 29 79

The in vivo antibody response to the lysozyme component of a lysozyme-lipopolysaccharide complex has been investigated in normal, thymectomized and nude mice. The splenic PFC response elicited by the complex in CBA mice is 10- to 20-fold higher than the response elicited by lysozyme admixed with LPS. Both lysozyme-LPS complexes and lysozyme + LPS mixtures prime mice for a subsequent secondary anti-lysozyme response. In contrast, thymectomized mice responded poorly to lysozyme-LPS complexes unless reconstituted with splenic T cells. However, nude mice responded as well as Nu/+ controls to the complex. The PFC response of normal and of nude mice was severely depressed by treatment with anti-lymphocyte serum. These findings suggest that T lymphocytes contribute significantly to the enhanced immune responsiveness associated with LPS administration.
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PMID:Immunologic properties of protein-lipopolysaccharide complexes. I. Antibody response of normal, thymectomized, and nude mice to a lysozyme-lipopolysaccharide complex. 30 94

The functional changes in splenic lymphoid populations from mice infected with T. brucei strain S42 were studied throughout the 3 weeks of infection. Within a week of infection, proliferation of B and T cells profoundly increased as shown by 3H-labelled thymidine incorporation and fluorescent staining of surface Ig; the spleen cells secreted high levels of both IgM and IgG immediately cells were put into culture; but with progressing infection this Ig production declined. The early effect on T cells was reflected by lack of responsiveness to PHA. B-cell potential was studied in low-density cultures treated with lipopolysaccharide (E. coli). Normal spleen cells proliferate extensively in these cultures with subsequent secretion of IgG as well as IgM. The ability to proliferate and produce Ig in response to LPS was severely depressed by day 7 and almost totally absent by day 12 of infection. Removal of T cells from the spleen cells obtained early in infection partly restored the response to LPS but as the infection neared its fatal end, B-cell potential appeared to become exhausted. Macrophages obtained from infected mice even early in infection profoundly depressed the ability of normal spleen cells to proliferate and secrete immunoglobulin in LPS cultures. The general immunodepressing effect of trypanosomes can be attributed to clonal exhaustion of B-cell potential caused by an undefined blastogenic stimulus from the parasites which may operate at least in part by the generation of suppressive T cells and macrophages.
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PMID:Suppressor cells and loss of B-cell potential in mice infected with Trypanosoma brucei. 30 69

Endotoxin (lipopolysaccharide, LPS) has been found to act on all three cell types of the immune system, thymus-derived (T-) cells, bone marrow-derived (B-) cells, and macrophages. LPS is mitogenic for B-lymphocytes and activates them to release a chemotactic lymphokine. Macrophage activation appears to be mediated by macrophage-activating factor, another lymphokine released from B-cells. In addition, LPS acts synergistically with phytohemagglutinin to initiate division of purified T-lymphocytes. All these phenomena are mediated by the lipid A moiety of LPS. The role of lymphoid cells in mediating the lethal effects of LPS have also been investigated. The adoptive transfer of spleen cells from LPS-responsive mice (C3H/HeN) to LPS-resistant but histocompatible mice (C3H/HeJ) rendered the LPS-resistant mice significantly more susceptible to LPS-induced lethality. These findings suggest that spleen cells play an essential role in mediating the lethal effects of LPS in vivo.
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PMID:Action of endotoxin on lymphoid cells. 30 90

The majority of adult B lymphocytes in the mouse bear two immunoglobulin isotypes, IgM and IgD (mu(+)delta(+) cells) (1). A small population of IgM-bearing cells lacks, or expresses very low levels of IgD (mu- predominant [mup] cells) (1). These cells are believed to constitute a less mature subset of B cells analogous to neonatal B cells (2). Based on the time during ontogeny when responses to T-independent (TI) and T-dependent (TD) antigens appear (3, 4) and the ability to block in vitro responses with anti- mu or anti-delta (5, 6, D. Mosier, personal communication), it has been suggested that the precursors of two TI-1 responses, trinitrophenyl (TNP)- Brucella (TNP-BA) and TNP-lipopolysaccharide (TNP-LPS) are mup cells (5, 6), whereas the precursor for a TD response, TNP-sheep erythrocytes (TNP-SRBC), bears both IgM and IgD (6). However, the possibility cannot be excluded that IgD is present on some or all of the TI precursors, but that it is not obligatory for triggering. In the present experiments we have examined the phenotypes of TI and TD precursors by treating cells with C' and either anti-mu or anti-delta before stimulation with antigen. Our results suggest that the majority of B cells that respond to TNP-BA, TNP-LPS, and TNP-SRBC bear IgD, even though in the case of the two TI antigens, IgD is not required for triggering.
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PMID:A dichotomy between the expression of IgD on B cells and its requirement for triggering such cells with two T-independent antigens. 31 18

The biologic activities of helper T cell-replacing factors derived from concanavalin A-stimulated murine T cells (TRF-T) and from lipopolysaccharide-activated macrophages (TFR-M) have been compared. TRF-T stimulates immune responses to heterologous erythrocyte antigens (SRBC and BRBC) in T cell-depleted spleen cultures but not in macrophage-depleted spleen cultures. TRF-M stimulates immune responses in both T cell-depleted and macrophage-depleted spleen cultures. Under conditions where LPS stimulates the release of TRF-M from cultures of activated macrophages, TRF-t has no effect on TFR-M production. Thus. TRF-T does not appear to function by stimulating the release of TRF-M from macrophages. In macrophage-depleted spleen cultures, saturating concentrations of TRF-T and TRF-M when mixed together exhibit striking synergistic effects on the induction of immune responses to erythrocyte antigens. The kinetics of the synergistic effects of TRF-M and TRF-T are consistent with an effect of TRF-M on the production of TRF-T sensitive B cells.
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PMID:Helper T cell-replacing factors secreted by thymus-derived cells and macrophages: cellular requirements for B cell activation and synergistic properties. 31 38


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