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)

The present study was undertaken to compare the effects of two adjuvants, SGP (a starch-acrylamide polymer) and Quil A (purified saponin), with that of aluminum hydroxide (Al(OH)3) on murine primary antibody responses to T-independent (TI) and T-dependent (TD) antigens. All three adjuvants augmented the responses to the TD antigens, dinitrophenyl-keyhole limpet hemocyanin (DNP-KLH), and sheep erythrocytes (SRBC). SGP was the most potent adjuvant and increased the primary IgG response to DNP-KLH as much as 90-fold. Quil A and Al(OH)3 had comparable effects on the primary response to DNP-KLH, but Quil A was less effective than Al(OH)3 for augmenting the primary response to SRBC. Quil A and SGP both augmented the primary IgM and IgG responses to trinitrophenyl-lipopolysaccharide (TNP-LPS), TNP-Brucella (TI-1 antigens), and TNP-Ficoll (TI-2 antigens). Al(OH)3, like most commonly used adjuvants, had little or no effect on responses to TI antigens. The kinetics of the response to TNP-Ficoll was altered by SGP, since peak responses were maintained for at least 7 days, while the response to TNP-Ficoll alone peaked on Day 4 and had declined considerably by Day 7. Both SGP and Quil A could augment responses to both optimal and suboptimal doses of antigen. The adjuvant activity of SGP was diminished, but still effective, when smaller amounts of SGP were used with the immunizing antigen, and all three adjuvants were able to augment primary responses when given in separate injections from the antigen. These results demonstrate that SGP is a very effective adjuvant, and show that both Quil A and SGP have a unique ability to increase antibody responses to TI antigens, suggesting that their effects may be mediated at least partially through B cells.
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PMID:Immunopotentiating effects of the adjuvants SGP and Quil A. I. Antibody responses to T-dependent and T-independent antigens. 348 57

The effect of single, sublethal i.p. injection of dieldrin on the primary antibody response to thymodependent (sheep red blood cells, SRBC) and T-cell-independent (lipopolysaccharide, LPS) antigens were investigated in inbred C57Bl/6 mice. Time-course studies showed significant suppression of the anti-SRBC IgM and anti-LPS IgM response at 7-24 days and at 4-14 days, respectively, after exposure to 0.6 LD50 of dieldrin. The anti-SRBC IgG response was also suppressed by dieldrin exposure, however, maximal suppressory effect was found at 48 days after the pesticide exposure. Similar patterns of the dieldrin-induced suppression of the primary IgM response to the thymodependent and T-cell-independent antigens, in addition to the overall control of cytotoxicity of lymphoid cell populations, suggest rather dysfunction of cellular cooperation during the inductory phase of the immune humoral response.
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PMID:Suppression of humoral immunity in inbred mice by dieldrin. 349 51

Enterotoxigenic Escherichia coli (ETEC) may have profound effects on the capacity of gut-associated lymphoid tissue to mount a secretory immune response because of the potential ability of heat-stable toxin or heat-labile toxin to modulate the immune response. To examine the effects of ETEC or its purified enterotoxins upon the humoral immune response of murine small intestinal Peyer's patch lymphocytes, BDF1 (lipopolysaccharide-responder) and C3H/HeJ (lipopolysaccharide-nonresponder) mice were orally primed with sheep erythrocytes (SRBC) four times during a 2-week period to initiate differentiation of Peyer's patch B lymphocytes to cells committed to anti-SRBC immunoglobulin A (IgA) production. Halfway through the oral priming regimen the mice were gastrically intubated with 10(8) ETEC, 10(8) non-ETEC, or saline. ETEC persisted in the small intestine for at least 7 days at a level of 10(3) to 10(4) bacteria per mouse. Seven days after the last oral dosing with SRBC, Peyer's patch lymphocytes were removed from infected or saline-treated mice and incubated in vitro with SRBC. The ETEC infection had a small effect on the anti-SRBC IgM plaque-forming cell response of SRBC-primed mice but inhibited significantly the anti-SRBC IgA plaque-forming cell response in both BDF1 and C3H/HeJ mice as compared with uninfected controls. The non-ETEC, an isolate from normal mouse small intestine, had no significant effect on either IgM or IgA anti-SRBC plaque-forming cell response. Purified heat-labile toxin, not heat-stable toxin, alone in a dose-dependent manner significantly inhibited both the IgA and IgM plaque-forming cell response of Peyer's patch lymphocytes from primed mice. These data suggest that ETEC can inhibit the development of the gut-associated lymphoid tissue IgA immune response through the immunopharmacological effect of an enterotoxin, the heat-labile toxin.
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PMID:Modulation of murine Peyer's patch immunoglobulin A response by enterotoxigenic Escherichia coli. 355 86

Humoral immunity of casein-treated B6C3F1 mice was evaluated. Splenocytes from casein-treated mice sensitized in vitro exhibited a marked suppression in their antibody response to the T-dependent antigen, SRBC (82%) and T-independent antigen, DNP-Ficoll (80%). In contrast, a control response to the polyclonal antigen, lipopolysaccharide (LPS), was observed. Cell fractionation and crossover reconstitution assays of adherent (ADH) and nonadherent (NAD) splenocyte populations from vehicle and casein-treated mice indicated that: 1) ADH splenocytes from casein-treated mice were responsible for suppression of humoral responses, 2) NAD splenocytes from casein-treated mice reconstituted with vehicle or naive ADH cells abrogated the immunosuppression, and 3) suppression of humoral responses in cultures containing casein ADH splenocytes was due to this cell populations inability to function as accessory cells in humoral responses rather than induction of suppressor macrophages. Results from in vivo studies with casein-treated mice sensitized with sheep red blood cells or dinitrophenyl-Ficoll paralleled the in vitro results.
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PMID:Inhibition of macrophage accessory cell function in casein-treated B6C3F1 mice. 362 70

Three pairs of chicken lines selected for high (H) and low (L) graft vs. host reaction (GVHR) competences, serum immunoglobulin G (IgG) levels, and antibody responses to Leucocytozoon caulleryi were examined for their immunocompetences and Marek's disease (MD) resistance. The GVHR-H and GVHR-L lines were further divided into two sublines according to their major histocompatibility B genotype. Immune responses to sheep erythrocytes (SRBC), bovine serum albumin (BSA), and a lipopolysaccharide (LPS) were compared between the high and low lines of each pair of selected lines. Significant differences were found in responses to SRBC and LPS in IgG-selected lines and in response to BSA in Leucocytozoon-selected lines. In all three instances antibody titers of the H line were higher than those of the L line. The GVHR competence expressed by the splenomegaly index (SI) was also significantly different between the H and L lines of all three selected-line pairs. The SI values in the GVHR-selected and IgG-selected lines were higher in the H line than in the L line, whereas those in the Leucocytozoon-selected lines were lower in the H line. Differences in MD incidence and in MD mortality were found between the GVHR-selected B11B11 subline and the IgG-selected lines. In both instances the L line was more resistant to MD than the H line.
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PMID:Immunocompetences and Marek's disease resistance in three pairs of chicken lines selected for different immunological characters. 362 59

1,25-Dihydroxyvitamin D3 and 1,24-dihydroxyvitamin D3 suppressed an antibody response to sheep red blood cells (SRBC, T cell-dependent antigen) by murine splenocytes, in concentrations ranging from 10(-10)-10(-7)M. These suppressive effects were markedly abrogated when T cell-depleted lymphocytes were cultured in the presence of a supernatant of concanavalin A-stimulated spleen cells. On the contrary, neither of them suppressed antibody response to trinitrophenyl-lipopolysaccharide (T cell-independent antigen). These results suggest that the suppressive effect of active vitamin D3 on anti-SRBC response was mediated by the inhibition of T cells.
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PMID:1,25-Dihydroxyvitamin D3 and 1,24-dihydroxyvitamin D3 suppress in vitro antibody response to T cell-dependent antigen. 387 58

The separation and properties of a new immuno-potentiator, Benincasa cerifera mitogen (BCM) fraction, were investigated. BCM fraction was separated from hot water extract of the seed of Benincasa cerifera Savi (Tohgashi) by gel filtration using Sepharose 4B. BCM fraction is a heteropolymer consisting of uronic acid, neutral sugars, protein, and phosphorus. The proliferation and differentiation of murine B cells were markedly stimulated by BCM fraction. The in vitro development of peritoneal macrophages into antitumor macrophages was also activated by the addition of BCM fraction to cultures. BCM fraction augmented the IgM and IgG antibody responses against sheep erythrocytes (SRBC) and the induction of delayed-type footpad reaction against SRBC. The antitumor activity of BCM fraction was observed in terms of prolongation of the survival period of mice bearing Meth A fibrosarcoma. After hydrolysis with 1% acetic acid at 100 degrees C for 4 h, marked mitogenic activity was found in a precipitate composed of 29% neutral sugars, 50% uronic acid, 1% protein, and 0.1% phosphorus. The precipitate did not contain detectable amino sugar. The possibility that the biological activities of BCM fraction may be due to contamination by bacterial lipopolysaccharide was ruled out on the basis of the results of chemical analysis and of marked mitogenicity noted in C3H/HeJ spleen cell cultures.
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PMID:Immunopotentiator separated from hot water extract of the seed of Benincasa cerifera Savi (Tohgashi). 387 10

Few immunomodulators are available for the control of infectious disease. One reason has been the lack of a suitable protocol for evaluating such agents. We have presented a series of assays of immune function that will allow a standardized approach to this problem. The value of this protocol has been established using long-term low dose, and short-term high dose, administration of bestatin, a small molecular weight microbial product. The experiments were done using both normal and immunocompromised animals. Bestatin had no effect on circulating leukocytes or the reticuloendothelial system. Leukocyte mobilization and T cell responsiveness in immunocompromised animals were enhanced following bestatin treatment. The antibody response to SRBC doubled in normal animals while the same treatment schedule resulted in a marked reduction in the response to Escherichia coli lipopolysaccharide. These results have established the value of the protocol and identified some new immunomodulating properties of bestatin which may be useful in the control of infectious disease.
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PMID:Immunopotentiation in infectious disease, I. Effect of bestatin on the immune response. 387 88

The action of a polysaccharide fraction obtained from hot water extracts of Angelica acutiloba Kitagawa, termed as Angelica immunostimulating polysaccharide (AIP) fraction, on murine lymphocytes participating in antibody responses was investigated. When AIP fraction was injected concomitantly into mice immunized with antigens, immunoglobulin M (IgM) and IgG antibody responses against sheep erythrocytes (SRBC) increased significantly, but IgM response against T-independent antigens such as trinitrophenylated lipopolysaccharide (TNP-LPS) and TNP-Ficoll did not augment. Murine B lymphocytes were polyclonally activated in vitro and in vivo by AIP fraction to differentiate into antibody-forming cells as functionally matured cells. The differentiation of B lymphocytes to an intermediate stage capable of responding to helper T lymphocytes was also stimulated by the administration of AIP fraction into CDF1 and C3H/HeJ mice. A concomitant injection of AIP fraction with SRBC for carrier priming resulted in the increment of anti-TNP IgM antibody response in cultured reconstituted with unprimed B and SRBC-primed T lymphocytes, indicating that AIP fraction can stimulate T lymphocytes.
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PMID:Lymphocyte activation by a polysaccharide fraction separated from hot water extracts of Angelica acutiloba Kitagawa. 387 57

The polyclonal immune response was induced in untreated mice and mice treated with cyclophosphamide by the administration of lipopolysaccharide from E. coli or S. marcescens. The number of cells forming antibodies to sheep red blood cells and to trinitrophenyl, and of cells producing immunoglobulins increased. The administration of LPS to mice pretreated with SRBC and CY (tolerant mice) considerably reduced the number of anti-SRBC AFC in comparison with the controls. The tolerogenic treatment did not change the number of anti-TNP AFC and IPC. Analogous results were obtained in genetically athymic (nude) mice and in B mice (thymectomized, lethally irradiated and reconstituted with embryonic liver cells). The results suggest that a deletion or a temporary inactivation of a fraction of the antigen-specific B cells occurs in tolerant mice. This inactivation cannot be explained by the absence of expression of surface immunoglobulins on B cells nor by the activity of suppressor T cells.
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PMID:Studies on lipopolysaccharide-induced polyclonal B cell activity in mice tolerized by sheep red blood cells and cyclophosphamide. 390 43


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