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

Preparations of Staphylococcus aureus strains Cowan 1 and Wood 46 and of lipopolysaccharide (LPS) were found to act as polyclonal B-cell-activating substances for human splenic and blood lymphocytes. All three substances induced polyclonal antibody secretion in blood and spleen cell cultures, as tested against fluorescein isothiocyanate-coupled sheep erythrocytes by a modification of the local hemolysis-in-gel assay. Antibodies were of IgM class, as shown by inhibition of plaque formation by anti-IgM but not by anti-IgG or anti-IgA antisera. All these substances also consistently induced the formation of intracellular immunoglobulin and increased DNA synthesis in stimulated spleen cells. In blood lymphocytes Staph. aureus Cowan 1 induced a consistent increase in DNA synthesis, whereas Staph, aureus Wood and LPS often gave low or no increase in DNA synthesis. Peak antibody formation was observed on day 3 in spleen cells and on day 6 in blood lymphocyte cultures. Stimulation into high-rate immunoglobulin secretion occurred with all PBAs also in B-cell-enriched cell suspensions but not in T-cell-enriched cells. Optimal responses were, however, always noted in unseparated cell suspensions. It is concluded that preparations of killed bacteria can be useful tools for the clinical evaluation of both specific and nonspecific antibody-forming ability in cells from different groups of patients.
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PMID:Polyclonal antibody secretion in human lymphocytes induced by killed staphylococcal bacteria and by lipopolysaccharide. 33 27

A heavy load of bacteria, referred to as dental plaque, accumulates at the junction between the teeth and gum. Bacterial plaque may be considered to have three functional components: (a) cariogenic organisms, (b) organisms inducing gingival inflammation and periodontal disease, and (c) adjuvant and tolerizing agents, such as lipopolysaccharides, dextrans and levans. Sequential investigation of plaque accumulation in man has shown a correlation between gingival inflammation and both lymphocyte transformation and macrophage migration inhibition. An adjuvant effect of in vivo plaque accumulation was manifested by the enhancement of T lymphocytes in the mixed leucocyte culture reaction and of B lymphocytes, as shown by the increased response to lipopolysaccharide. It may be significant that a substantial component of bacterial plaque consists of dextrans and levans, produced by certain streptococci and actinomyces, and lipopolysaccharides from Gram-negative bacteria. These bacterial products are B cell mitogens which may have an adjuvant or tolerizing effect on immune responses. The relationships between immunogenicity, mitogenicity, adjuvanticity and tolerogenicity of lipopolysaccharides, levan and dextran have not been clearly defined. However, important variables of the polyglycans are the molecular weight, type of branching, negative charge, epitope density, degradability, dosage and the sequence between mitogen and antigen. Dental plaque in man is a focus of B cell mitogens and T cell antigens which may modulate the immune responses in such a way as to induce a protective response in the development of caries and a damaging response in periodontal disease.
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PMID:Immunological responses to bacterial plaque in the mouth. 34 20

A linear dependence of the response to the thymus-dependent antigen (log of the plaque-forming cell count) on the T cell dose at the initial curve section was observed in syngeneic transfer of T and B cells mixture. The exponential slope differed for T cells of different origin and could serve as the measure of helper activity. In case of an excess of T-lymphocytes the response reaches the maximum, whose level is independent of the organic origin of T cells. By the helper activity T cells are distributed in the following order: T cells of the spleen and cortisone-resistant thymocytes greater than T cells of the lymph nodes greater than cortisone-sensitive thymocytes. There was established a quantitative equivalence by the capacity to activate B cells between the T-lymphocytes and E. coli lipopolysaccharide.
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PMID:[Comparative assessment of the efficacy in humoral response of T-cells of various organ origin and their substitutes]. 35 86

The effect of autologous normal mouse serum on activating properties of the polyclonal B cell activators lipopolysaccharide and purified protein derivative was studied. 'Low' concentrations (0.1-1%) were found to be slightly stimulatory, whereas 'high' concentrations (greater than 10%) were clearly inhibitory both for the induction of plaque-forming cells and for the DNA synthetic response. Similar effects were recorded in unstimulated cultures. Absorption of normal mouse serum with the erythrocytes used as target cells in the plaque assay resulted in less suppression or sometimes even in enhanced responses.
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PMID:Regulation of lymphocyte activation by serum factors. 37 29

Unfractionated spleen cells, B cells from normal mice, and nu/nu spleen cells respond to the addition of bacterial lipopolysaccharide (LPS) and T-cell-replacing factor (TRF) by production of plaque-forming cells (PFC) in excess of the number expected from the addition of LPS and TRF separately. This synergistic activity is dependent on the presence of the antigen, SRBC. Supernatants of both allogeneic spleen cell mixtures and spleen cells cultured with Con A are effective and synergize best at concentrations suboptimal for their ability to act as TRF alone. Culture supernatants of unstimulated normal or fractionated cell populations are ineffective. Synergy is not dependent on the presence of macrophages in the cultures. Purified LPS free from active contaminants, as well as commercially available LPS, show synergy with TRF. Synergy was seen when TRF was added at initiation of culture or 24 hr later. It is suggested that synergy is the equivalent of LPS adjuvant activity, that the role of T cells in LPS adjuvanticity is that of a conventional cooperating cell, and the LPS acts as an adjuvant by inducing B cells to become more sensitive to T cell helper factors.
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PMID:Synergy between T cell-replacing factor and bacterial lipopolysaccharides (LPS) in the primary antibody response in vitro: a model for lipopolysaccharide adjuvant action. 37 17

Purified protein derivative (PPD) of tuberculin was found to induce antibody secretion and DNA synthesis in human lymphocytes from blood, spleen, tonsil and lymph node. Antibody secretion was measured as plaque-forming cells (PFC) against fluorescein isothiocyanate (FITC) coupled sheep red blood cells (SRBC) in a haemolysis-in-gel assay. Peak antibody secretion by 100 micrograms/ml of PPD was usually seen on day 6 for blood lymphocytes, and varied from day 3 to day 6 for spleen cells. Peak DNA synthesis for blood lymphocytes stimulated by various concentrations of PPD ranged from day 4 to day 7. The highest number of PFC in tonsil and spleen cells was induced by PPD compared to Staphylococcus aureus bacteria Cowan 1, lipopolysaccharide (LPS) and pokeweed mitogen (PWM). Antibody secretion by PPD was not affected when phagocytic cells were removed by iron treatment. PPD stimulated a higher DNA synthesis in unseparated lymphocytes or mixtures of T and B cells than in enriched T or B cell suspensions. PPD did not induce PFC in B cells enriched by the removal of sheep erythrocyte rosette-forming cells (E-RFC). However, more PFC were stimulated by PPD in enriched E-RFC compared to unseparated lymphocytes, which may indicate that most of the FITC-SRBC reactive B cells also form rosettes with SRBC.
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PMID:Antibody production and DNA synthesis of human lymphocyte subpopulations induced by PPD tuberculin. 38 83

Data is presented comparing the activities of three immunosuppressive agents, cyclosphosphamide, frentizole and azathioprine in models of humoral immunity in mice. Cyclophosphamide and frentizole suppressed the primary and secondary plaque forming cell responses to sheep erythrocytes at lower doses than did azathioprine. Prolonged suppression of serum antibody titers occurred following short-term therapy with cyclophosphamide or frentizole, but not azathioprine. Azathioprine was also the least effective agent in suppressing a primary response to the T-independent antigen, trinitrophenylated lipopolysaccharide. All three agents were found to inhibit the induction and activity of suppressor cells at immunosuppressive doses.
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PMID:Comparative effects of azathioprine, cyclophosphamide and frentizole on humoral immunity in mice. 40 16

Antibody response to a T-cell dependent antigen, sheep erythrocytes and to a B-cell mitogen, purified lipopolysaccharide (LPS), has been studied in mice kept on protein deficient (2 and 4 per cent casein) diets. The number of plaque-forming cells (PFC) to SRBC were 20-5 +/- 7-7 per million spleen cells in protein-deficient animals compared to 261-0 +/- 31-1 in parallel controls maintained on a protein rich diet (18 per cent casein). No difference was observed in number of PFC formed in controls and deficient animals to LPS, values were 161-4 +/- 19-7, 158-5 +/- 14-2, & 162-3 +/- 31-9 in control (18 per cent casein) and deficient groups (4 per cent and 2 per cent casein) respectively. The delayed hypersensitivity skin reaction to SRBC measured in foot pads was significantly lower in mice on 4 per cent casein diet compared to controls. These studies suggest that the effect of protein deficiency is primarily on T-cell function and not on the B-cell response;
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PMID:Depression of T-cell function and normality of B-cell response in protein calorie malnutrition. 40 30

Receptors for phages specific to Pseudomonas aeruginosa strain PAO were studied. Phages 16, 44, 109, F8, and PBI are lipopolysaccharide (LPS) specific as shown by neutralization tests. The PhI50's of the LPS, adsorption rate constants with strain PAO and the plaque morphologies of these five phages were quite similar. Phages 1214 and 7 also appear to be LPS-specific on the basis of host-range studies. Phage 73 is pilus-specific, while phages 21 and 68 fall into a group which does not attach to pili, flagella, or LPS. A theoretical approach to the interpretation of phage-cell interactions is presented.
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PMID:The nature of Pseudomonas aeruginosa strain PAO bacteriophage receptors. 40 24

Various subcellular bacterial fractions are known to enhance immune responses and serve as potent adjuvants. Muramyl dipeptide (MDP), a synthetic adjuvant mimicking a component of mycobacterial cell walls, enhances humoral immunity to soluble antigens and can increase macrophage cytotoxicity toward mastocytoma cells in vitro. In the present study MDP was found to enhance the hemolytic antibody plaque response of normal mouse spleen cells in vitro to SRBC at a level equal to or greater than that induced by Escherichia coli lipopolysaccharide. Furthermore, MDP was found to enhance the antibody response to SRBC nonspecifically in unimmunized spleen cell cultures, suggesting that similar to LPS the synthetic dipeptide may induce a generalized clonal expansion of committed lymphocytes and thus serve as a "polyclonal activator." MDP also enhanced the immune responsiveness of normal splenocytes to suboptimum concentrations of SRBC, indicating that this material may be useful in enhancing immunity in situations where there would normally be a poor immune response.
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PMID:Stimulation of an enhanced in vitro immune response by a synthetic adjuvant, muramyl dipeptide. 41 67


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