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

Spleen cells from newborn mice do not respond by proliferation to concanavalin A (Con A) or bacterial lipopolysaccharide (LPS) stimulation. This non-reactivity cannot be reversed to a positive response by exogenous interleukin-2 (IL-2). The stimulation with Con A of spleen cells from newborn mice, in contrast to cells from adult animals, does not result in synthesis of mRNA for inducible 55,000 molecular weight (MW) IL-2 receptors (IL-2R). The failure of neonatal spleen cells to synthesize IL-2R mRNA is an intrinsic property of the cells themselves, and it is not due to activity of natural suppressor cells present in newborn animals. Since the expression of functional IL-2R represents one of the early and pivotal events in immune cell activation, we propose that the inability to synthesize IL-2R may be one of the primary reasons for the immunological immaturity of newborns.
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PMID:Inability of mitogen-stimulated spleen cells from newborn mice to synthesize interleukin-2 receptors. 227 35

Leptospiral lipopolysaccharides (LPSs) extracted from Leptospira interrogans serovars copenhageni and hebdomadis were tested for the biological effect to mouse B, T and NK cells. Each leptospiral LPS was a potent mitogen for spleen B cells. Activation of the cells was also expressed by polyclonal B cell activation. In contrast, mitogenicity for T cells, induction of interleukin-2 (IL-2) secretion in T cells and increase of tumor-killing activity and chemiluminescence in NK cells were not observed after stimulation with leptospiral LPS. After intravenous injection of leptospiral LPS in mice, the spleen and lymphnodes were examined by histocytochemical technique. Increase of Ig-bearing lymphocytes was recognized while decrease of T cells was observed in the lymphoid organs. Mitogenic response to PHA, Con A and PWM decreased with relation to the T cell depletion. In conclusion, it is apparent that leptospiral LPS possess marked immunological potencies on B cells but not T and NK cells. The biological effects of leptospiral LPS were common ones as LPS but the level was considered to be different from classical LPS such as Escherichia coli LPS.
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PMID:Biological effects of leptospiral lipopolysaccharide to mouse B, T and NK cells. 228 May 2

Based upon an immunomodulatory role for Corticotropin-Releasing Factor (CRF), a low molecular weight neurohormone, we investigated the effect of CRF on the production of interleukin-1 (IL-1) and interleukin-2 (IL-2) activities of mononuclear cells isolated from the peripheral blood of healthy subjects. The production of both IL-1 and IL-2 was stimulated by a nanomolar concentration of CRF by itself. In addition, CRF augmented the production of IL-1 as induced by lipopolysaccharide and the production of IL-2 as induced by phytohemagglutinin. These results suggest that CRF modulates the function of the cells of the immune system presumably by acting as a blood-borne mediator of the neuroendocrine-immune pathways.
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PMID:Enhancing effect of corticotropin-releasing neurohormone on the production of interleukin-1 and interleukin-2. 229 2

The effect of mouse seminal vesicle fluid (SVF) on blastogenic response of splenocytes to mitogens was investigated. SVF significantly suppressed blastogenic response of splenocytes to concanavalin A and phytohemagglutinin in a dose-dependent manner, but blastogenic response to lipopolysaccharide was suppressed only at low, although significant, levels, even at high concentrations of SVF. Extensive dialysis did not reduce the capacity of SVF to inhibit blastogenesis of splenocytes. For elucidation of the mechanisms of suppression of blastogenic response, interleukin-2 (IL-2)-dependent cells were cultured in the presence of IL-2 and various concentrations of SVF. The presence of SVF did not inhibit the proliferative response of IL-2-dependent cells to IL-2. These results suggest that the suppression of blastogenic response of T lymphocytes to mitogens in seminal plasma is caused by an undialyzable component (or components) derived from seminal vesicle and is attributable to the alteration of receptors for mitogens or of IL-2 receptors that are expressed on stimulation by mitogens.
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PMID:Biological functions of mouse seminal vesicle fluid. I. Suppression of blastogenic responses of lymphocytes. 232 11

Rat antisera raised against supernates derived from draining lymph node cells of skin-graft-primed mice exhibit a number of immunosuppressive effects in vitro and in vivo. The skin graft-induced, cell-free-supernates had been demonstrated to contain a number of helper activities that led to an antigen-specific induction of cytolytic T lymphocytes and/or to the induction of interleukin-2 synthesis. The rat antisera administered to skin graft recipients resulted in prolongation of major-histocompatibility-complex-incompatible skin graft survival. The rat antisera appear to have a specificity for the inhibition of T cell responses in vitro, although binding to B and T cells was apparent. The responses of unprimed cells to T cell mitogens and alloantigens are blocked, whereas B cell responses to the lipopolysaccharide mitogen are not blocked by the antisera. The generation of cytolytic T lymphocytes and the cytolytic functions of such cells are both blocked by the rat antisera. The inhibition of the differentiation pathway in cells cultured continuously with the antisera was overcome only through the addition of conditioned medium obtained from stimulated concanavalin A rat spleen cells, as opposed to mouse cell conditioned media. The rat antisera do not appear to block T cell responses via the IL-2 receptor, and were found to be substantially less effective against activated and proliferating T cells. These rat antisera have allowed us to further examine the pathways involved in T cell responses.
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PMID:Immunosuppressive activities of rat antisera raised against supernates from skin-graft-primed cells. 241 94

The antineoplastic drug bleomycin, which has not been shown to have immunosuppressive activity, was tested for its effect on concanavalin A-induced interleukin-2 production. When the drug was added to splenocytes of Lewis rats or Balb/c mice in the presence of concanavalin A, in optimal conditions for interleukin-2 production, no detectable effects were seen. However, using a suboptimal dose of concanavalin A, bleomycin increased interleukin-2 release significantly. This effect was achieved using less than 1 microgram/ml bleomycin. In addition, bleomycin was tested for its ability to alter interleukin-1 production by peritoneal exudate macrophages. The drug seems to increase the release of interleukin-1 from peritoneal exudate macrophages of Lewis rats without any lipopolysaccharide added or with a suboptimal concentration of lipopolysaccharide. It is suggested that bleomycin, and probably other cytotoxic drugs, may modulate the immune response through its effects on the release of immunostimulating cytokines such as interleukin-1 and -2.
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PMID:Potentiation of release of interleukin-2 by bleomycin. 242 40

The priming effect of endogenous biological response modifiers (BRMs), interferons (IFNs), and interleukin-2 (IL2), and the triggering effect of BRMs of bacterial origin, OK-432 and Corynebacterium parvum, on endogenous production of the tumor necrosis factor (TNF) were investigated in mice. TNF activity in serum was measured by in vitro cytotoxicity assay with L-929 cells as a target. The i.v. injection of OK-432 (3KE per mouse) triggered TNF maximally (mean value: 30 U/ml) after 2 h, with a similar time course to that of triggering by lipopolysaccharide. The priming activities of IFNs and IL2 were examined in the system of TNF-triggering by OK-432. The i.v. injection of recombinant IFN-gamma (rIFN-gamma, 10(4) U per mouse) increased TNF production to 790 U/ml; this priming effect was observed just after its injection, was maximal after 2 to 6 h, and disappeared after 24 h. Other types of interferon, rIFN-alpha A/D(Bgl) (2 X 10(5) U per mouse), rIFN-beta (10(6) U per mouse), and natural IFN-alpha/beta (10(6) U per mouse) showed maximal priming activity 6 h after their injection (200 to 800 U/ml) but no effect just after their injection. Recombinant IL2 (10(6) U per mouse) had priming activity that showed a similar time course to that of interferons other than IFN-gamma (a maximal TNF production: 100 U/ml). The i.v. injection of C. parvum, like OK-432, triggered TNF production at doses of 0.06 and 0.3 mg per mouse 2 h after its injection and the triggered TNF activity was enhanced by rIFN-gamma. These findings suggest that combinations of the above endogenous BRMs as priming agents and OK-432 or C. parvum as a triggering agent could induce endogenous production of TNF even in human cancer patients. In fact, combined administration of rIFN-gamma and OK-432 produced TNF in human cancer patients. The advantage of this method for treatment of human cancer patients is discussed.
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PMID:Endogenous production of tumor necrosis factor in normal mice and human cancer patients by interferons and other cytokines combined with biological response modifiers of bacterial origin. 244 26

Interferon (IFN)-induced tryptophan degradation, catalyzed by indoleamine 2,3-dioxygenase (IDO), has been shown to mediate antimicrobial activity in epithelial cells. IDO activity has also been augmented in peripheral blood mononuclear cells (PBMC) treated with IFN or interleukin-2 (IL-2). The effector cells in this population have now been further characterized. PBMCs were isolated from normal donors, separated into monocyte and lymphocyte populations by plastic adherence, treated with IFN or IL-2, and cultivated in medium supplemented with [3H]tryptophan. Culture supernatants were collected after a 48-h incubation and fractionated by high-performance liquid chromatography; radioactivity was determined in fractions corresponding to tryptophan and its metabolites. IFN-gamma and IFN-beta induced IDO activity only in monocytes (plastic-adherent, nonspecific esterase-positive PBMCs). The induction of IDO activity by IL-2 required both monocytes and lymphocytes. Interaction was required between these populations for induction of IDO by IL-2, due to production of IFN-gamma by T lymphocytes, with subsequent IFN-gamma-mediated induction of IDO in monocytes. A number of myeloid cell lines as well as monocyte-derived macrophages were also tested for their ability to be induced to degrade tryptophan in response to IFN treatment. Monocyte-derived macrophages were found to retain their capacity to be induced by IFN-gamma and IFN-beta to degrade tryptophan after differentiation, and to possess seven times more IDO activity per cell than IFN-induced monocytes. However, the presence of lipopolysaccharide (LPS) in the culture medium was required for the maximum induction of IDO activity by IFN-beta. Furthermore, higher concentrations of LPS were sufficient to induce IDO activity in macrophages in the absence of exogenous IFN.
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PMID:Interferon-induced indoleamine 2,3-dioxygenase activity in human mononuclear phagocytes. 246 22

The immunopotentiating activities of lipopolysaccharide from Achromobacter stenohalis (A-LPS) were examined. A-LPS was structurally atypical and gave no endotoxin shock in A-LPS-inoculated mice. Analysis in vitro showed that A-LPS was a potent activator of both macrophages and B-lymphocytes. After macrophage stimulation with A-LPS, interleukin-1 (IL-1) secretion, interferon (IFN) production and chemiluminescence (CL) response were induced. A-LPS was a potent mitogen for spleen lymphocytes. However, induction of interleukin-2 (IL-2) secretion in T lymphocytes was not observed. These activities of A-LPS were similar to or higher than that of enterobacterial LPS.
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PMID:Biological effects of lipopolysaccharide from Achromobacter stenohalis on lymphocytes and macrophages. 248 63

We developed a sensitive bioassay system for the determination of tumor necrosis factor-alpha (TNF) using HEp-2 adherent human epipharynx carcinoma cells as targets. TNF from separated human monocytes was triggered by lipopolysaccharide (LPS). In a 24 hr 3H-thymidine incorporation assay, TNF-like activity was seen to reproducibly destroy radiolabeled target cells, i.e., inhibits thymidine incorporation and causes detachment of adherent HEp-2 cells. HEp-2 cells were insensitive to human interleukin-1 (IL-1) and interleukin-2 (IL-2). In contrast, human interferon-alpha and gamma were also cytotoxic for target cells. Monocyte supernatants stimulated by LPS, however, failed to contain detectable amounts of interferons.
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PMID:A simple assay for tumor necrosis factor using HEp-2 target cells. 248 15


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