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 effects of some dopaminergic antagonists were investigated on mouse lymphocyte proliferative responses in vitro. The mixed D1/D2 dopaminergic antagonists chlorpromazine, haloperidol and flupentixol inhibited 3H-Thymidine incorporation into adult BALB/c mouse spleen cells stimulated by concanavalin A, lipopolysaccharide from Escherichia coli, and allogenic cells in a mixed lymphocyte reaction. The inhibition was achieved at concentrations greater than 10(-6) M. It was not accounted for by decreased cell viability and it was no longer demonstrable when the compound was added 24 h or 48 h after the mitogenic stimulus. Conversely selective D2 dopaminergic antagonists sulpiride, metoclopramide and domperidone had no inhibitory effect at concentrations ranging from 10(-9) to 10(-5) or 10(-4) M. The three mixed D1/D2 antagonists inhibited the mitogenic effect of interleukin-1 on concanavalin A-stimulated thymocytes, but not the activity of interleukin-2 on the proliferation of the CTLL-2 cell line. The mixed D1/D2 antagonists interfered with the production of interleukin-2 but not with that of interleukin-1. These results indicate that dopaminergic antagonists may differentially affect lymphocyte proliferative responses to T or B cell mitogens or alloantigens. The mechanisms involved in terms of receptor specific or non specific phenomenons are discussed.
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PMID:Differential effect of mixed D1/D2 and selective D2 dopaminergic antagonists on mouse T and B lymphocyte proliferation and interleukin production in vitro. 290 53

The suppression of contact hypersensitivity (CHS) after a single exposure to ultraviolet (UV) radiation provides an excellent model system with which to study both the activation and the mode of action of suppressor T cells. Suppression of CHS after UV radiation is mediated by hapten-specific suppressor T cells (UVTs). These cells have a broad range of activity: CHS and antibody production in vivo and the generation of cytolytic T lymphocytes (CTL) and T-cell proliferative responses in vitro are suppressed by UVTs. The present study is concerned with determining the target of UVTs. The UVTs could suppress the response to hapten-modified T-dependent antigens, such as trinitrophenyl (TNP)-modified sheep erythrocytes (TNP-SRBC) or TNP-conjugated bovine serum albumin (TNP-BSA), but had no suppressive effect on the response to a T-independent antigen, TNP-conjugated lipopolysaccharide (TNP-LPS). The UVTs also suppressed the generation of interleukin-2 (IL-2) in vitro. The suppression of CTL generation in vitro and CHS in vivo could be overcome by the addition of exogenous IL-2. These data suggest that UVTs suppress the immune response by affecting T-helper cell function.
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PMID:The effect of ultraviolet radiation-induced suppressor cells on T-cell activity. 295 84

The cyclic undecapeptide cyclosporine A (CsA) is a potent immunosuppressive agent that inhibits the initial activation of T lymphocytes. This agent appears to be most effective in blocking the action of mitogens such as concanavalin A and the calcium ionophore A23187, which cause an influx of Ca2+, but not those that may act by alternate mechanisms. These observations suggest that CsA may block a Ca2+-dependent step in T cell activation. We have shown that stimulation of the T3-T cell receptor complex-associated Ca2+ transporter activates the Na+/H+ antiport (Rosoff, P. M., and L. C. Cantley, 1985, J. Biol. Chem., 260: 14053-14059). The tumor-promoting phorbol esters, which are co-mitogenic for T cells, activate the exchanger by a separate pathway which is mediated by protein kinase C. Both the rise in intracellular Ca2+ and intracellular pH may be necessary for the successful triggering of cellular activation. In this report we show that CsA blocks the T3-T cell receptor-stimulated, Ca2+ influx-dependent activation of Na+/H+ exchange, but not the phorbol ester-mediated pathway in a transformed human T cell line. CsA inhibited mitogen-stimulation of interleukin-2 production in a separate cell line. CsA also inhibited vasopressin stimulation of the antiporter in normal rat kidney fibroblasts, but had no effect on serum or 12-O-tetradecanoyl phorbol 13-acetate stimulation. CsA did not affect serum or vasopressin or serum stimulation of normal rat kidney cell proliferation. CsA also had no effect on lipopolysaccharide or phorbol ester stimulation of Na+/H+ exchange activity or induction of differentiation in 70Z/3 pre-B lymphocytes in which these events are initiated by the protein kinase C pathway. These data suggest that mechanisms of activation of Na+/H+ exchange that involve an elevation in cytosolic Ca2+ are blocked by CsA but that C kinase-mediated regulation is unaffected. The importance of the Na+/H+ antiport in the regulation of growth and differentiation of T cells is discussed.
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PMID:Cyclosporine A inhibits Ca2+-dependent stimulation of the Na+/H+ antiport in human T cells. 301 82

The time course of immune modulation induced by acute treatment with O,S,S-trimethyl phosphorodithioate (OSS-TMP), an impurity in technical formulations of malathion, was examined in female C57BL/6 mice. The immune parameters studied included the generation of cytotoxic T lymphocytes (CTL) to alloantigen (H-2 incompatible) and antibody secreting cells to sheep red blood cells, proliferative response to the mitogens, and interleukin-2 (IL-2) production. Acute administration of the non-toxic doses of OSS-TMP, i.e. 20 or 40 mg/kg, led to an elevation in the generation of a CTL response on day 1 or 7, respectively. At 20 mg/kg OSS-TMP, the antibody response was elevated at day 3. However, at a dose of 40 mg/kg OSS-TMP, the antibody response was suppressed at day 1 following treatment. Following acute administration of 60 or 80 mg/kg OSS-TMP, the generation of an antibody and CTL responses was suppressed at all time points tested with 1 exception. One day following treatment at a dose of 60 mg/kg OSS-TMP, there was no change in the CTL response. At day 7 following treatment, the mitogenic responses to lipopolysaccharide and phytohemagglutinin were elevated at all doses of OSS-TMP administered. At this time point, however, the proliferative response to Concanavalin A was elevated in a dose dependent manner. IL-2 production was suppressed following acute administration of 60 or 80 mg/kg OSS-TMP at all time points tested and at all doses tested on day 5 following treatment. These data indicate that OSS-TMP, unlike its congener, O,O,S-trimethyl phosphorothioate, enhances the generation of humoral and cell mediated immune responses of C57BL/6 mice following administration of non-toxic doses.
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PMID:Effects of acute administration of O,S,S-trimethyl phosphorodithioate on the generation of cellular and humoral immune responses following in vitro stimulation. 305 16

Bacterial endotoxin (lipopolysaccharide, LPS) and interleukin-2 (IL-2) are known to stimulate NK cell mediated cytotoxicity against tumor cells. In the present report we sought to correlate the stimulatory effect of LPS and IL-2 on NK cell activity with ultrastructural changes which occurred as a result of such stimulation. Peripheral blood mononuclear cells (PBMC) were purified from healthy donors by a Ficoll-Hypaque density gradient technique. Leu-11a+ NK cells were isolated by flow microfluorometry using a monoclonal FITC conjugated anti-Leu-11a antibody and a FACS II cell sorter. The PBMC were incubated, respectively, with E. coli LPS or recombinant IL-2 (IL-2) for various time periods. Sorted Leu-11a+ NK cells were incubated with LPS for 24 hours. The NK cytotoxicity in the PBMC and sorted Leu-11a+ cells was assessed by a 51Cr release technique using K562 tumor cells as targets. Leu-11a+ NK cells were identified by immunoelectron microscopy using anti-Leu-11a antibody and labeling with horseradish peroxidase or colloidal gold. Results showed that both LPS and IL-2 significantly enhanced the cytotoxic activity of PBMC. The cytotoxicity of sorted Leu-11a+ cells was augmented by LPS. Recombinant IL-2 induced a significant increase in the number of dense granules, hypertrophy of Golgi apparatus and rough endoplasmic reticulum, and mitosis of Leu-7+ cells and Leu-11a+ cells 4 or 7 days after stimulation. These data indicate that: (1) the effect of LPS on the enhancement of NK cytotoxicity in PBMC may be a direct and/or indirect process involving production of lymphokines; (2) LPS has a direct effect on sorted Leu-11a+ cells; (3) IL-2 stimulates mitosis of Leu-7+ cells and Leu-11a+ cells; and (4) the LPS or IL-2 induced ultrastructural changes in Leu-11a+ cells are consistent with the enhanced NK cytotoxicity.
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PMID:Ultrastructural and functional effects of lipopolysaccharide and interleukin-2 on human NK cells. 305 78

T cell derived cytokines, interleukin-2 and interferon-gamma, are known to upregulate the interleukin-1 synthesis of monocyte/macrophages. The effect of a third T cell derived cytokine, interleukin-4, was now investigated. Human peripheral blood monocytes were activated with bacterial lipopolysaccharide in the presence or absence of interleukin-4 and the production of biologically active interleukin-1 was quantitated both from the culture supernatants and from the monocyte lysates using the mouse thymocyte assay. Interleukin-4 had a clear dose-dependent suppressive effect on the interleukin-1 synthesis. IL-1 alpha and IL-1 beta mRNA levels, quantitated by Northern blot analysis, were equally high in the lipopolysaccharide plus interleukin-4 supplemented cultures and in the cultures with lipopolysaccharide alone, suggesting that the effect of interleukin-4 in the interleukin-1 biosynthesis is post-transcriptional.
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PMID:Interleukin-4 inhibits interleukin-1 synthesis by a posttranscriptional mechanism. 306 82

Muramyl dipeptide (MDP) and lipopolysaccharide (LPS) were effective in augmentation of killer cells generation from human peripheral blood mononuclear cells (PBMC) in response to recombinant human interleukin-2 (IL-2). Pretreatment of PBMC with combination of LPS and MDP resulted in most significant their proliferation stimulated by IL-2. Thus our results show the enhancement of PBMC sensitivity to IL-2 by action of LPS, MDP and most of all by their combination in vitro.
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PMID:[The stimulating action of lipopolysaccharide and muramyl dipeptide on the activation of mononuclear cells in human peripheral blood by recombinant interleukin-2 in vitro]. 306 97

A study was conducted on the activity exerted by prolonged dietary supplementation with progressive amounts of retinoids on cell-mediated immune responses and the growth of transplantable tumors in mice. A few groups of BALB/c mice received 0 (group C), 50 (group A 50), 200 (group A 200), 500 (group A 500), and 1,000 (group A 1000) IU retinol palmitate/mouse/day in drinking water for 150 days. At progressive intervals mice from each group were tested for proliferative responses to concanavalin A (Con A), Escherichia coli lipopolysaccharide, interleukin-2, and interferon-gamma release to Con A. Ten mice from each group were also challenged with the 90-100% tumor-inducing dose of 3 distinct transplantable tumors. At the end of the experiment the principal organs were histologically examined, and the accumulation of vitamin A was evaluated. In groups A 200, A 500, and A 1000, an increase in the proliferative responses and production of lymphokines as compared to those in group C occurred after 60-90 days, but vanished after 150 days. The takes of the 3 tumors were impaired when the challenges were performed on days 75 and 150. This enhancement of distinct functions of cellular reactivity and resistance to transplantable tumors showed a linear relationship with the amount of supplemental retinol palmitate for the first 60-90 days. After 150 days, however, these enhancement effects vanished or tended to decrease.
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PMID:Effect of prolonged administration of low doses of dietary retinoids on cell-mediated immunity and the growth of transplantable tumors in mice. 308 48

Proteose-peptone-induced intraperitoneal neutrophils from rats were activated in terms of tumor cytotoxicity by pretreatment with culture supernatants from a human T cell leukemia line, Jurkat (culture sup). Culture sup-treated neutrophils showed cytotoxicity against various tumor cell lines. The cytotoxicity of culture sup-treated neutrophils was dependent on the number of neutrophils and the concentration of culture sup. Cytostasis by activated neutrophils was observed very early in the assay incubation period (within 6 hr), but cytolysis first occurred at 24 hr after the start of incubation. Factor(s) in culture sup responsible for the activation of cytotoxic neutrophils were stable to temperature and pH treatments, and their molecular weight was higher than 10,000. The responsible factor(s) for activation of cytotoxic neutrophils were different from interleukin-2, serum-derived factor, and bacterial lipopolysaccharide.
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PMID:A T cell leukemia line produces factor(s) that render rat neutrophils cytotoxic. 309 56

Lymphocyte growth and differentiation are controlled by signals resulting from the interaction of antigen and cellular products, such as lymphokines, with specific cell membrane receptors. Resting B lymphocytes can be activated by low concentrations (1-5 micrograms/ml) of antibodies to membrane IgM, which is the B-lymphocyte receptor for antigen. The binding of anti-IgM to B cells causes a rapid increase in intracellular free calcium concentration ([Ca2+]i), in inositol phosphate concentration, and in protein kinase activity. Moreover, the effects of anti-IgM on B cells are mimicked by the combined use of calcium ionophores and phorbol esters. Since phorbol esters activate protein kinase c, this suggests that the increase in [Ca2+]i and in phosphatidylinositol metabolism stimulated by anti-IgM are critical events in B-cell activation. The entry into S phase of B cells stimulated with anti-IgM depends on the action of a T-cell-derived factor designated B-cell stimulatory factor (BSF)-1. This is a 20,000-Da protein which is a powerful inducer of class II major histocompatibility complex molecules. Although an important cofactor for B-cell proliferative responses to anti-IgM, its major locus of action is on resting B cells. B cells stimulated with anti-IgM and BSF-1 do not synthesize secretory IgM. However, if two additional T-cell-derived factors, B151-TRF and interleukin-2, are added to cultures, a substantial proportion of stimulated B cells produce secretory IgM. BSF-1 has also been shown to participate in the "switch" in Ig class expression. Resting B cells cultured with lipopolysaccharide will switch to IgG1 secretion in the presence of purified BSF-1.
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PMID:Regulation of B-lymphocyte activation, proliferation, and immunoglobulin secretion. 309 4


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