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

Lipid A isolated from lipopolysaccharide of Yersinia pseudotuberculosis was used for immunization of rabbits to afford antisera to lipid A with titers of 1:640 in the passive hemolysis test. Exhaustion of immune serume with sheep erythrocytes decreased antibody titers up to 1:160. Authentic samples of 2-(DL-3-hydroxytetradecanoyl)amino-2-deoxy-D-glucose 6-phosphate, 2-tetradecanoylamino-2-deoxy-D-glucose 6-phosphate and 2-acetamido-2-deoxy-D-glucose 6-phosphate have been synthesized in order to carry out a comparative study of inhibitory activity of these compounds and lipid A using a system of lipid A and antiserum to lipid A. As a result, the immunodominant moiety of the lipid A of Y. pseudotuberculosis proved to contain a D-glucosamine residue acylated with 3-hydroxytetradecanoic acid at the amino group. The nature of the fatty acid acylating the amino group of glucosamine does not play an important role in the structure of immunodominant moiety of lipid A.
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PMID:Structural studies on the immunodominant group of lipid A from lipopolysaccharide of Yersinia pseudotuberculosis. 8 32

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

In order to enhance general reactivity of immune system in the tumor-bearing host, we employed extract of Cordyceps sinensis (CSE) as a biological response modifier. Cordyceps sinensis is an interesting material produced by a kind of mushroom parasitic to larval moths and was used to hasten recovery from exhaustion in ancient China. In this experiment, C57BL/6 mice implanted subcutaneously with syngeneic EL-4 lymphoma cells were employed as the host. Oral administration of the extract leads to a reduction of tumor size and prolongation of the host survival time. As judged by plaque-forming cells against T-dependent (sheep erythrocytes) and T-independent (bacterial lipopolysaccharide) antigens, CSE showed to augment the antibody responses. As for the activities of peritoneal macrophages, chemotaxis was dramatically depressed within a few days after EL-4 transplantation up to the end of life, but treatment with CSE at -14, -7, -4, +4, +7 and +10 days after the tumor transplantation augmented the activity about four times stronger than that of control. Phagocytic activity of macrophages was also decreased in tumor-bearing mice treated with cyclophosphamide (100 mg/kg) 3 and 5 days after tumor transplantation. But administration of CSE restored the activity to more than the normal level. The overall efficacy of CSE was tested with protective activity against systemic infection by Salmonella enteritides. The tumor-bearing mice receiving this medicine lived significantly longer than any other groups without CSE.
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PMID:Augmentation of various immune reactivities of tumor-bearing hosts with an extract of Cordyceps sinensis. 220 72

In previous works, we have postulated the existence of an immunological equilibrium between persistence of the antigen presence and the B-cell maturation-differentiation; from this hypothesis, it follows that the antigen presence induces the IgM to IgG switch and the final exhaustion of the response which persists if the antigen stimulation persists. On the basis of those results, we have considered of interest to study the direct and indirect polyclonal activation of the background of murine plaque-forming cells (PFC), against sheep erythrocytes. We have investigated this activation by different doses of mitogens, which activate B cells, thus producing various cellular proliferations. The goal was to find out whether polyclonal activation increased the background (as expected) but did not change the IgM/IgG PFC ratio, probably because of a lack of antigenic stimulation. As mitogens, we have used: E. coli lipopolysaccharide (LPS), a known polyclonal activator of B cells which causes a proportional increase in the number of background plaque-forming cells to a given antigen, and pokeweed mitogen (PWM) which, although less frequently used, has been shown to stimulate both T and B lymphocytes. Female Swiss albino mice have been used; 10 mice per group for both control and test groups. The mitogens were administered according to the following doses and protocol: LPS-1 dose of 10, 50 or 100 micrograms; 3 doses of 10, 50, or 100 micrograms (1 dose per week). PWM-1 dose of 50, 100 or 200 micrograms; 3 doses of 50 or 100 micrograms (1 dose per week).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Polyclonal stimulation activates the basal level of IgM and IgG plaque-forming cells against sheep erythrocytes without inducing a change from IgM to IgG]. 353 63

The kinetics of allohelp mediated by diffusable factors revealed that help by nonirradiated T cells (TOR) peaked at 48 to 72 hr, followed by a sharp decline if the T cells remained in the cultures. The temporal decrease in help after 72 hr was not mediated by suppressor lymphokines because mixtures of early (24 to 48 hr) and late (120-hr) allogeneic supernatants enhanced help synergistically. Lyt-1, Ia- T cells mediated the temporal decline in help and suppressed allogeneic B cell activation in co-cultures, and this "down-regulatory" activity (allosuppression) was radiosensitive. Help by irradiated T cells (T1000R) increased gradually until it plateaued between 96 and 120 hr. The helper activities of the allogeneic supernatants were directly proportional to their T cell growth factor (TCGF) activities. In addition, their kinetics were identical, and the removal of TCGF from 48-hr allogeneic supernatants by adsorption with TCGF-dependent HT-2 cells depleted both helper and TCGF activities. Help was restored to depleted 48-hr and 120-hr allogeneic supernatants by preparations of TCGF obtained from concanavalin A (Con A)-stimulated FS6-14.13 hybridoma cells that were adsorbed with lipopolysaccharide (LPS)-activated B cells or normal spleen cells (NS), but not with HT-2 cells. These results indicate that allohelp is dependent on TCGF. Moreover, help was dependent on at least one factor in addition to TCGF, because a high level of synergy occurred between TCGF and the "help-deficient" 120-hr allogeneic supernatant. In conclusion, the mechanism whereby Lyt-1, Ia- T cells regulated B cell activation with positive and negative allogeneic effects was through the production and subsequent exhaustion of TCGF, respectively. The production of TCGF and help was radioresistant, but exhaustion of TCGF and suppression was radiosensitive.
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PMID:The allogeneic effect: the mechanism of allosuppression by Lyt-1, Ia- T cells. 623 81

The effect of a monoclonal anti-delta antibody on the in vitro B cell response to the B cell mitogen lipopolysaccharide (LPS) has been studied. Titration of anti-delta antibody in mass cultures stimulated by LPS resulted in a dose-dependent reduction of thymidine incorporation. IgM and IgG plaque forming cell (PFC) responses were poorly affected at high concentration, and slightly increased at low concentrations of anti-delta antibody. By limiting dilution analysis it was shown that anti-delta antibody inhibit 30-50% of LPS-reactive B cells to grow as IgM secreting clones, while increasing the average size of clones that grew in the presence of anti-delta as compared to control cultures. Anti-delta also results in increased frequencies of IgG secreting clones. By immunofluorescence it was possible to show the presence of a higher relative number of cells containing immunoglobulin as an effect of anti-delta antibodies. Observations made at early times of culture indicate that the cells that do not proliferate in the presence of anti-delta undergo an early maturation to secretion. Experiments performed on LPS blasts suggest that the effects of anti-delta on cell proliferation require the presence of antibodies at early times in the response, while the effects on maturation can be manifested during clonal development. The relevance of membrane IgD and of the IgM-to-IgD ratio in the maintenance versus exhaustion of the clone is discussed.
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PMID:Effect of anti-delta antibodies on clonal expansion and maturation of B lymphocytes. 697 5

This study was initiated to determine the effect of physical exercise on the in vivo tumor necrosis factor-alpha (TNF) response to Escherichia coli lipopolysaccharide (LPS). Rats familiarized with treadmill running and surgically implanted with vascular catheters were either not exercised or exercised to near exhaustion (mean run time of 102 +/- 13 min) before intravenous LPS challenge (1 mg/kg; lethality of dose is 10-20% in 24 h). Compared with time-matched nonexercised control rats, exercised rats had increased heart rates, plasma lactate, and plasma corticosterone and decreased plasma glucose at the conclusion of exercise. In response to LPS, both groups became hypotensive, exhibited transient hyperglycemia, and sustained hyperlactacidemia. By 30 min post-LPS, plasma corticosterone levels were similar in the two groups. Nonexercised rats exhibited a normal plasma TNF response to LPS with the peak value (10,400 +/- 2,000 U/ml) occurring 90 min after LPS challenge. In contrast, the TNF response in rats exercised before LPS administration was blunted to 17% of the nonexercised group, with the peak occurring at an earlier time after LPS. Addition of recombinant murine TNF to postexercise plasma was fully expressed. The TNF response remained attenuated when LPS was administered up to 6 h after completion of exercise, but it returned to normal in rats allowed to recover for 24 h. The results demonstrate that exercise, perhaps as a stress modality, markedly suppresses the systemic TNF response that is normally observed in response to LPS challenge.
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PMID:Prior exercise suppresses the plasma tumor necrosis factor response to bacterial lipopolysaccharide. 783 63

The effects of exercise training and acute exercise on the immune system were investigated in rats. For chronic exercise training, the rats ran on a drum exerciser at the intensity of about 60-70% of maximal oxygen consumption (VO2max) for 30 min and then extended up to 60 min per day, 5 days per week for 10 weeks. The rats were at rest for 3 days before sacrifice. The mitogenic activity of spleen lymphocytes to concanavalin A (Con A) and staphylococcal enterotoxin B (SEB) decreased as compared to the sedentary control, while proliferative response to lipopolysaccharide (LPS) increased. The interleukin-2 (IL-2) production in the training group was reduced. The immunomodulatory effect after acute exercise has also been investigated and it showed profound enhancement of cell proliferation to Con A, SEB and LPS in mild (50% VO2max for 10 min) and moderate (70% VO2max for 10 min) exercise groups. The enhancing activity was less prominent after severe exercise (> 75%) VO2max until exhaustion). The IL2 production increased in all of these acute exercise groups. Nevertheless, there was no significant variation between exercise and control groups in the cell number per spleen and the percentages of various lymphocyte populations, i.e., total T, CD4+, CD8+ and IL-2R+ T cells as well as B cells. In summary, this study indicates that chronic exercise training may cause the reduction of T cell activity while acute exercise manifests an enhancing effect. However, B cell proliferation was elevated in both chronic and acute exercise groups.
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PMID:The effect of chronic and acute exercise on immunity in rats. 846 30

We have previously demonstrated an altered pattern of tumor necrosis factor (TNF) secretion in patients with familial Mediterranean fever (FMF). To examine whether TNF determination could assist in diagnosing FMF, we stimulated heparinized blood of 51 asymptomatic FMF patients with lipopolysaccharide (LPS) and then measured TNF production in response to inducers, compared to unstimulated blood cells and to cells from a control group of 12 matched healthy subjects. Following LPS pretreatment, which induced TNF release, FMF patients produced significantly less TNF than controls, whether production was 'spontaneous' or induced by either LPS or phytohaemagglutinin (p < or = 0.003). Such 'exhaustion' did not occur in untreated cells. We then used these results to classify a further group of 29 FMF patients and 10 matched healthy controls ('validation' group) who underwent the same studies. The test correctly identified 25/29 patients as having FMF and 7/10 controls as not having FMF; a sensitivity of 86% and a specificity of 70% (likelihood ratios 2.9 (positive test) and 0.2 (negative)). Identification of a blunted TNF response following previous stimulation by a simple assay, may help the diagnosis of FMF in asymptomatic patients, provided it is interpreted in conjunction with supportive clinical data.
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PMID:Induced TNF production in vitro as a test for familial Mediterranean fever. 873 64

To prime immune responses, dendritic cells (DCs) need to be activated to acquire T cell stimulatory capacity. Although some stimuli trigger interleukin 12 (IL-12) production that leads to T helper cell type I (TH1) polarization, others fail to do so and favor TH2 polarization. We show that after activation by lipopolysaccharide, DCs produced IL-12 only transiently and became refractory to further stimulation. The exhaustion of cytokine production impacted the T cell polarizing process. Soon after stimulation DCs primed strong TH1 responses, whereas at later time points the same cells preferentially primed TH2 and nonpolarized T cells. These findings indicate that during an immune response, T cell priming conditions may change in the lymph nodes, suggesting another mechanism for the regulation of effector and memory T cells.
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PMID:Kinetics of dendritic cell activation: impact on priming of TH1, TH2 and nonpolarized T cells. 1101 2


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