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

The T-cell regulatory function has been evaluated in lines of mice genetically selected according to the High (H) and Low (L) antibody responsiveness to heterologous erythrocytes. The inhibition of antibody production following CD4+ subset depletion was stronger in L than in H mice. The dose of CD4-specific monoclonal antibody (MoAb) needed for a 50% inhibition of the anti-sheep erythrocyte antibody response was much lower in L mice, even when their responsiveness was improved by repeated antigen injections or by co-injection of lipopolysaccharide as an adjuvant. Lymph-node cells from L mice responded normally or even better than those from H mice to in vitro non-specific triggering via lectins, exogenous superantigens or CD3-specific MoAb. In contrast, the antigen-specific responses of the lymph-node cells from protein-primed mice were consistently lower in the Low responder mice. Altogether the results suggest that a defective stimulation of T helper lymphocytes by the antigen contributes to the weak antibody response of L mice.
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PMID:Specific and non-specific T-cell activation in high and low antibody-producing mice (selection IV-A). 787 90

When B cells from BALB/c mice were cultured with lipopolysaccharide (LPS) and interleukin-4 (IL-4), a large amount of IgE was detected in the culture supernatants. The IgE production from unseparated spleen cells cultured with LPS and IL-4 was less than the amount of IgE obtained from separated B cells. When syngeneic T cells were added to separated B cells cultures, which were subsequently stimulated with LPS and IL-4, less IgE was produced, as compared to cultures without T cells. The hypothesis that T cells, or factors secreted by these cells, inhibit IgE production is supported by the fact that the degree of suppression of IgE production paralleled the number of T cells added. CD8(+)-enriched T cells were slightly more suppressive than CD4(+)-enriched T cells. Addition of exogenous IL-3 was only partially suppressive. These observations suggest that IL-4 added to unseparated spleen cells in vitro stimulates B cells for IgE production and also stimulates T cells. Lymphokines secreted by these stimulated T cells may in turn act on B cells. Some of these lymphokines, such as interferon-gamma and IL-2, may have a suppressive action on IgE production.
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PMID:Suppression of IgE production in unseparated spleen cell cultures. 790 2

We have recently shown that donor CD4-enriched cells of Th2 cytokine phenotype, generated by treating mice in vivo with a combination of interleukin-2 (IL-2) and IL-4, prevent lipopolysaccharide-induced, tumor necrosis factor-alpha-mediated lethality during graft-versus-host reaction. To assess the potential regulatory role of such Th2-type cells in lethal graft-versus-host disease (GVHD) and graft rejection, we used a fully allogeneic murine transplant model using sublethally irradiated hosts (B6-->C3H, 500 cGy). Such recipients generated a strong host-versus-graft response, as reflected by their ability to reject T-cell-depleted inocula. The administration of T-cell-containing donor whole spleen inocula resulted in alloengraftment, but such recipients developed lethal GVHD. However, mice receiving sequential donor whole spleen (day 0) and CD4-enriched, Th2-type (day 1) populations engrafted, and had prolonged survival with protection from histologically defined tissue injury associated with GVHD. The findings in this fully allogeneic model thus extend our previous observations and indicate that the transfer of donor Th2-type cells may be an important strategy for regulating GVHD. Furthermore, the sequential "Th1(-)-->Th2-type" donor cell transfer described in this report represents a novel approach for abrogating graft rejection with concomitant control of GVHD and illustrates the importance of kinetics in the interaction of functionally distinct donor T-cell populations.
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PMID:Donor CD4-enriched cells of Th2 cytokine phenotype regulate graft-versus-host disease without impairing allogeneic engraftment in sublethally irradiated mice. 794 9

An inflammatory reaction, essential for defence against infection and for wound repair, may also induce irreversible tissue damage. It appears that the central nervous system has developed its own immunosuppressive strategy in order to limit the destructive effects of inflammation. To clarify this point, we have characterized in one unique model of inflammation induced in the rat by intracerebral lipopolysaccharide injection the kinetics of the inflammatory reaction, the participation of immunitary and glial cells and of three growth factors. Among these molecules, brain-derived neurotrophic factor mRNA expression was found decreased following LPS injection. No striking differences were observed in the brain parenchyma after stab lesion or inflammatory lesion apart from an increase in the number of monocytes/macrophages recruited early to the lesion area. Macrophages were later accumulated around the lesion when astroglia and microglia reactions occurred. Some of the macrophages and microglia expressed major histocompatibility complex class II antigens on their surface whereas no T or B lymphocytes were observed in the brain parenchyma. However, a subpopulation of CD3- and CD4-negative CD8-positive cells, likely natural killer cells, was observed around the lesion site; this recruitment was inhibited by the highest dose of LPS. This study therefore supports the hypothesis of a suppression of some aspects of cell-mediated immunity in the brain, mechanisms which need to be further characterized.
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PMID:Lipopolysaccharide intracerebral administration induces minimal inflammatory reaction in rat brain. 798 42

Millions of people have been exposed to silicones because of the widespread use in consumer products such as cosmetics and toiletries, food products, household products and paints. Silicones have wide use in medical practice, including lubricants in tubing and syringes, and as implantable devices. The most prevalent silicone in medical use is polydimethylsiloxane. This study was undertaken to determine the subchronic immunotoxicologic potential of the principal constituents of breast implants: silicone fluid, silicone gel and silicone elastomer. An alternative covering for devices containing silicone gels, polyurethane, was also included in the study. Silicone fluid and gel were injected subcutaneously into female B6C3F1 mice (1 ml/mouse) and 6 mm disks of silicone elastomer or polyurethane were implanted subcutaneously. There were no treatment-related deaths or overt signs of toxicity. None of the tested materials had notable effects on body or organ weights, erythrocytes or leukocytes in the blood, blood chemistries such as alanine aminotransferase, urea nitrogen, glucose, albumin or total protein. The cellularity of the bone marrow and responses to CSF-GM and CSF-M were normal. The tested silicones did not alter the distribution of B cells and T cells in the spleen, but polyurethane perturbed the distribution of CD4+CD8+ and CD4-CD8- T cells. The antibody response to sheep erythrocytes was not markedly altered, nor were proliferative responses to concanavalin A, phytohemagglutinin, lipopolysaccharide or allogeneic cells. Reticuloendothelial function was normal, but polyurethane evoked an enhanced phagocytosis of Covaspheres by adherent peritoneal cells. Natural killer cell activity and serum complement were not altered. All silicone materials afforded modest protection to a challenge with Listeria monocytogenes that killed 40 to 58% of control mice. Host resistance to Streptococcus pneumoniae or the B16F10 tumor was not affected by any of the treatments. There is a pattern indicative of some perturbation of T cell differentiation in mice implanted with a polyurethane disk.
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PMID:Subchronic 10 day immunotoxicity of polydimethylsiloxane (silicone) fluid, gel and elastomer and polyurethane disks in female B6C3F1 mice. 798 83

The effect of renal function on cytokine secretion capacity of mononuclear cells was analysed in patients who had not been subjected to any form of renal replacement therapy. The aim of the study was especially to determine whether there is a defect of monocyte function. The patients were divided into three groups of 12 on the basis of renal function: group I, serum creatinine 1.5-3 mg/dl; group II, 3-6 mg/dl; and group III, > 6 mg/dl. Serving as controls were 36 age- and sex-matched healthy volunteers. IL-1 beta, IL-6, TNF-alpha, IL-2 and IF-gamma concentrations were measured in the supernatants of stimulated and unstimulated cells isolated from the blood. Renal function was not found to have any effect on the secretion capacity of IL-2 and IF-gamma. However, the secretion capacity of IL-1 beta of lipopolysaccharide (LPS)-stimulated monocytes was reduced in patients of group III to 214 +/- 290 pg/ml, compared with 501 +/- 327 pg/ml in controls (P = 0.047). The effect was even more accentuated for IL-6 (group III: 5422 +/- 5116 pg/ml; controls: 16,319 +/- 12,474 pg/ml; P = 0.019). Spontaneous secretion levels did not change for any of the cytokines, and LPS-stimulated TNF-alpha secretion was also normal. Highly purified blood monocytes/macrophages were stained for CD14, HLA-DR, CD11c, and CD4. Neither the percentage of positive cells nor the fluorescence intensity, as measured by FACS, was influenced by renal function, and no correlation could be established between function and phenotype.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of renal function on cytokine secretion of monocytes and lymphocytes. 809 Mar 29

Injection of murine recombinant interleukin-3 (IL-3) into (C57BL/10 x DBA/2)F1 mice, sublethally irradiated with 300 cGy and killed 14 days later, induced in the thymus recovery of the cell number and mitotic responsiveness to concanavalin A (Con A), as well as an increase in number of double-negative CD4-CD8-, double-positive CD4+ CD8+, and single-positive CD4+CD8- and CD4-CD8+ cells. Also in the spleen, the cell count and mitotic responsiveness to Con A and lipopolysaccharide were increased to normal levels by IL-3 treatment. If the assays were performed 21 or 28 days after irradiation, IL-3 treatment was able to restore thymus and spleen cell counts as well as T- and B-cell mitotic responsiveness, even when mice were exposed to 400 or 500 cGy, respectively. These results altogether indicate that IL-3 induces differentiation and growth of thymocytes and recovery of T- and B-cell functions in mice exposed to sublethal irradiation.
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PMID:Murine recombinant interleukin-3 induces recovery of T and B cells in irradiated mice. 812 46

Although patients with refractory periodontitis have been widely reported, no clear biologic profile of these patients has been noted. The purpose of the present study was to evaluate host responsiveness of a well-defined group of refractory periodontitis patients by determining the effect of a lipopolysaccharide (LPS) challenge on monocyte surface receptor density and on the release of inflammatory mediators. Venous blood was obtained from 7 refractory periodontitis, 8 stable periodontal maintenance, and 8 gingivitis patients with no evidence of periodontitis. Mononuclear cells were cultured in either control media or media treated with Actinobacillus actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), or Salmonella typhimurium (S. typh) LPS. At 0 and 24 hours supernatants were assayed for prostaglandin-E2 (PGE2) and interleukin-1 beta (Il-1 beta) release by ELISA. Using flow cytometry the density of specific monocyte surface receptors were assayed with Mo3e and LeuM3 monoclonal antibodies (mAb); T-cell CD4/CD8 ratios were assayed with OKT-3, OKT-4, and OKT-8 mAb. After 24 hours incubation with Pg or S. typh LPS, the upregulation of the Mo3e receptor was significantly decreased for refractory periodontitis patients (P < 0.05) when compared to gingivitis and to stable maintenance patients. In refractory periodontitis patients the T-cell CD4/CD8 ratio was decreased. Upon stimulation with Pg or S. typh LPS, monocytes from stable maintenance and refractory periodontitis patients released more Il-1 beta (P < 0.05) and PGE2 (P = 0.13 and 0.15) than monocytes from gingivitis subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Host responses in patients with generalized refractory periodontitis. 813 19

The alterations of cytokines (TNF,PGE2), plasma lipopolysaccharide and their prognostic influences in 58 patients with intra-abdominal infection were observed with ELISA and RIA. The effect on physiopathologic process with herbal purgation method was explored. The results showed that as the level of plasma LPS raised the serum TNF, plasma PGE2 elevated obviously and the cellular immunity inhibited elevated in treatment and control groups. There was a linear positive correlation between the plasma LPS and the serum TNF in control group. Between the plasma PGE2 and CD4 lymphocytes of peripheral blood, it existed a linear negative correlation in treatment group. After two treatment courses, the recovery of abnormal indexes in treatment group was earlier than that in control group accompanied by escalation of lessened toxicity rate of LPS, more rapid in reducing the level and detectable rate of serum TNF, and the lowering of complication rate successively and the inhibition of cellular immunity tended to be relieved in treatment group.
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PMID:[Lipopolysaccharide-induced cellular immunity response and effect of herbal purgation method in intra-abdominal infection]. 821 74

While lipopolysaccharide endotoxin is the most prominent inducer of the kinecascade (TNF alpha, IL-1, 4, 6, 8) that leads to shock and multiple organ failure, bacterial exotoxins and products of certain gram positive bacteria can induce the same end results. We theorize that more than one pathogen can induce the sequence of protooncogene activation and growth factor release that results in the formation of KS. If KS has its own unique viral etiology, this virus has not as yet been isolated or identified but we continue to search for it. However, it is entirely possible that these lesions do not have a single well-defined etiologic agent but are the result of multiple agents cooperating in a set sequence. An endogenous, or apathogenic exogenous, retrovirus may replace HIV for initiator growth factor induction in CD4 cells in the classical (Mediterranean) or iatrogenic disease; and other pathogens co-exist or sequentially replace each other in the African endemic disease; whereas an array of viral pathogens (prominent among them CMV) take over growth factor induction in endothelial cells proliferating in response to the initiator growth factor (oncostatin M) released from HIV-infected CD4 lymphocytes in AIDS-KS.
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PMID:Multiple pathogens may induce growth factor cascade resulting in KS. 823 2


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