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)

A concurrent study of specificity, regulation, ontogeny, and genetics of murine natural killer (NK) cell and natural antibody (NAb) activities [in DBA/2, CBA/J, A/Sn, and A/J inbred mice, Bg/Bg + mice of the inbred C57BL/6J background, (C57BL/6 x DBA/2) F1 mice, and (CBA x DBA/2) F1, (A/Sn x DBA/2)F1, and (A/J x DBA/2)F1 mice] revealed that : a) The expressions of NAb and NK cell specificities associated with the YAC-1 tumor were directly related and could not be distinguished on the basis of inhibition and absorption studies, whereas the expressions of the specificities associated with a second NK cell-sensitive tumor, the SL2 lymphoma, were not directly related. b) Treatment of mice with the adjuvants proteose peptone and lipopolysaccharide or the interferon inducers polyinosinic-polycytidylic acid and 2-amino-5-bromo-6-methyl-4-pyrimidinol resulted in increases in NAb levels and NK cells, which suggested that certain aspects of the regulation of these activities may be similar or the same. c) High NK cell activity was codominantly inherited and high serum NAb levels were recessive, which argues against the theory that the NK cell receptor is a passively acquired NAb. d) NK cell activity declined with increasing age in contrast with NAb levels that remained constant throughout adult life. e) Bg/Bg mutants that exhibit an NK Cell defect expressed normal levels of NAb. Despite the differences in their genetics, murine antitumor NAb and NK cells bear certain common features-in particular, their response to microbial products and interferon inducers and at least a portion of antigen repertoire against which they are directed.
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PMID:Genetics, regulation, and specificity of murine natural antitumor antibodies and natural killer cells. 694 81

The role for lipopolysaccharide (LPS) and a pristane-induced peritoneal exudate (PIPE) on the in vitro development of murine plasmacytoma was studied. MOPC-315 cell suspensions showed little tendency for colony formation in a soft agar culture medium. Additions of LPS and PIPE were required for maximal colony formation. The LPS effect was dose-dependent down to nanogram quantities. PIPE prepared from inbred strains of mice not susceptible to pristane-induced plasmacytoma (DBA/2) or from normal peritoneal washings was ineffective. PIPE activity was radioresistant and not transferable by cell-free conditioned medium. Three strains of transplantable plasmacytomas showed colony formation stimulation by LPS plus PIPE, but LPS and PIPE were ineffective with lymphosarcoma P1798.
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PMID:Lipopolysaccharide and pristane-induced peritoneal exudate requirements for plasma tumor cell colony formation. 695 Jan 64

Peritoneal exudate macrophage monolayers (PEMM) from C57BL/6 and DBA/2 mice inoculated ip with tumor allografts were induced to release in vitro labile cell toxin(s), herein called "macrophage cytotoxin(s)" (MCT). Macrophages released MCT spontaneously for a short interval when initially established as monolayers, and they were reinduced to secrete MCT by exposure to allogeneic and syngeneic tumor cells (but not to normal cells) and by exposure to polyinosinic-polycytidylic acid (poly I . poly C) and lipopolysaccharide (LPS). PEMM from normal mice treated ip 3 days previously with thioglycollate were also induced to release toxins in vitro. These cells did not release MCT spontaneously before or after treatment with neoplastic cells but were induced to release MCT by exposure to poly I . poly C or LPS. Resident peritoneal macrophages did not release MCT either spontaneously or after treatment with tumor cells, poly I . poly C, or LPS. MCT released from alloimmune mice stimulated with syngeneic or allogeneic tumor cells were resolved by molecular sieving into a major peak at 140,000--160,000 daltons, called "alpha-MCT," and into a minor peak at 60,000 daltons, called "beta-MCT." However, supernatants from thioglycollate-induced PEMM, stimulated with poly I . poly C or LPS, appeared to be composed entirely of the alpha-class. alpha-MCT from poly I . poly C-stimulated PEMM caused 31--56% lysis of syngeneic EL-4 and allogeneic L-929, NS-1, and YAC-1 tumor cells in vitro but was not cytotoxic for normal cells. Secretion of the MCT by PEMM derived from thioglycollate-treated animals stimulated with poly I . poly C was inhibited by colchicine, emetine, iodoacetic acid, trypan blue, and cytochalasin B.
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PMID:Inducible macrophage cytotoxins. I. Biokinetics of activation and release in vitro. 695 64

Treatment of DBA/2J mice bearing a T1699 syngeneic mammary adenocarcinoma (Ts) with a single intraperitoneal (i.p.) injection of 100 ug melphalan produced complete tumor regression in about 65% of the animals treated; however, tumors recurred in about 85% of these regressors after 15-25 days' remission. The drug regimen was ineffective against Ts tumors growing in immunosuppressed or immunodeficient animals. Stimulation of immunologically intact Ts tumor-bearers with bacterial lipopolysaccharide (LPS) or with phytohemagglutinin (PHA) 3 days prior to melphalan therapy, on the other hand, produced not only higher rates of tumor regression but also significant increases in the number of permanent cures. A tumor induced by T1699 subline TR2 was resistant to the same regimen, although Ts and TR2 cells were equally susceptible to the cytotoxic and growth-inhibiting activities of the drug in vitro. In contrast, the combination of specifically armed monocytes and melphalan in vitro produced enhanced killing of Ts cells but not of TR2 cells. Analysis of the collaborative cytotoxicity between immune effector cells and melphalan indicated that exposure of tumor cells to killer cells increased the drug susceptibility of the tumor cells, but not the reverse. These results suggest a possible mechanism for in vivo resistance of tumors to chemotherapeutic agents that is not directly associated with the drug resistance of the tumor cells in vitro.
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PMID:Collaboration between specific anti-tumor immunity and chemotherapeutic agents. 696 55

NZB mice bearing the CBA/N X chromosome linked defect were generated by repetitive backcrossing and selection of the Xid gene. The male offspring resulting from the cross of NZB with CBA/N were selected as being XidY on the basis of sera IgM and IgG3 levels and responsiveness to DNP-Lys-Ficoll. Following this inbreeding protocol, 6th generation backcross NZB XidY mice were compared to littermate controls with respect to B cell function. Sera immunoglobulin levels of IgG1, IgG2b and IgA were similar in XidY and XY mice. In contrast, levels of IgM and IgG3, from XidY mice were approximately 15% and 50%, respectively, of values found in littermates. Furthermore, XidY mice failed to respond to DNP-Lys-Ficoll and had less than 3% splenic Lyb 5.1-bearing cells. Splenic immunoglobulin cell surface profiles, obtained by the fluorescent activated cell sorter, indicated a significant reduction in the frequency of Ig bearing cells in Xid animals. Such profiles were similar to those obtained for spleen cells from reference control CBA/N mice. Finally, an elevated number of splenic, lymph node and bone marrow background and lipopolysaccharide-induced B cell clones in semi-solid phase agar was found in NZB but not C57BL/6, C3H, BALB/c and DBA/2 controls. In contrast, NZB XidY mice had virtually no detectable B cell colonies. This data, obtained on significantly inbred XidY NZB mice, suggests that the Xid gene is dominant over several aspects of polyclonal B cell activation in NZB mice and indicates that serial observation of these mice will be valuable in understanding the interactions of genetic immunologic mutations and cellular function in autoimmunity.
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PMID:Study of congenitally immunologic mutant New Zealand mice. V. B cell function of NZB-Xid mice. 697 4

DBA/2 mouse spleen cells were stimulated in vitro by (a) alloantigen (mitomycin-treated CBA/J splenocytes), (b) the T cell mitogen concanavalin A (Con A), and (c) the B cell mitogen lipopolysaccharide (LPS). The cultures were pulsed for 10 h with (14)C-labeled galactose and glucosamine. Radiolabeled glycosphingolipids (GSL's) were extracted from the cells and the neutral GSL's isolated and analyzed by high-performance thin-layer chromatography. Two of the radioactive neutral GSL's, 9 and 12a, were found to be prominent in the alloantigen-stimulated cells but not in T cells stimulated by Con A. GSL 9 was also present as a minor component in LPS-stimulated B lymphocytes. GSL's 9 and 12a were purified by preparative column chromatography on Iatrobeads. The sequence and anomeric linkages of the carbohydrate moiety of these glycolipids were determined by successive degradation with exoglycosidases. The structures were shown to be Gal(alpha1-x)Gal(beta1-x)GlcCer (glycolipid 9) and GalNAc(beta1-x)Gal(alpha1-x)Gal(beta1-x)GlcCer (glycolipid 12a), respectively. The latter glycolipid may serve as a marker for alloantigen-activated T cell subpopulations.
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PMID:Structure elucidation of marker glycolipids of alloantigen-activated murine T lymphocytes. 697 20

To determine whether the existence of anti-dsDNA producing lymphocyte clones is limited to autoimmune strains of mice, spleen cells derived from autoimmune mice (NZB, NZB X NZW F1, MRL) and from normal strains (BALB/c, DBA/2, C57BL/6, C3H/eb) were cultured with E. coli lipopolysaccharide (LPS). DNase-treated supernatants from these cultures were assayed for anti-dsDNA antibodies by employing a sensitive solid-phase radioimmunoassay with poly (dA-dT) as the antigen. All tested spleen cells secreted a small yet significant amount of anti-dsDNA upon stimulation with LPS. There was no difference in the amount or in the heavy chain type of anti-dsDNA secreted by cells from normal and autoimmune strain cells. Evidence of clonal expansion in unstimulated cells was observed only in cultures prepared from older autoimmune animals. Removal of T cells from the spleen cell preparations had no marked effect on the spontaneous or stimulated antibody secretion. Anti-dsDNA antibodies could also be induced in vivo by i.p. injection of LPS into young normal animals. Splenocytes from all tested strains spontaneously secreted anti-ssDNA and anti-TNP antibodies in culture, and these were present at relatively high levels in the serum of unstimulated animals. Stimulation with LPS increased secretion of anti-ssDNA and anti-TNP in all strains in vitro and in five of seven strains in vivo as well. It can be concluded that a) the existence of anti-dsDNA-producing clones is not limited to autoimmune strains, and b) these clones are expanded in old but not in young autoimmune mice. They are not expanded in normal mice at any age.
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PMID:The in vitro and in vivo induction of anti-double-stranded DNA antibodies in normal and autoimmune mice. 697 78

Immune reactivity of primiparous pregnant C57Bl/6J mice was investigated using in vitro assays of mitogen reactivity. The response to the T cell mitogens phytohemagglutinin (PHA) and concanavalin A of cells from the paraaortic (PA) lymph nodes, which drain the uterus, was decreased in pregnant animals. Reactivity to lipopolysaccharide, a B cell mitogen, was normal. The decreased PHA response was seen with PA cells from mice bearing syngeneic or allogeneic (to DBA/2J) fetuses. It was not due to a change in sensitivity to PHA dose or to active suppression (as demonstrated by mixing experiments). Phytohemagglutinin reactivity of cells from inguinal nodes of pregnant mice showed a more variable depression of response in comparison to that seen with cells from the draining PA nodes. The response of axillary and brachial node cells was similar to virgin values. Statistical analysis revealed no differences in the average number of PA lymphocytes or fetuses per mouse between mice bearing syngeneic or allogeneic fetuses. This parallels the similarities found between syngeneic and allogeneic matings in in vitro functional assays. This study demonstrates that pregnant mice (syngeneic or allogeneic) show only a decrease in T proliferative capacity localized to the area of the uterus, while such responses in the rest of the body are left essentially intact.
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PMID:Cellular immunity during pregnancy. II. Response to T and B cell mitogens. 697 82

Bacterial lipopolysaccharide (LPS) and sheep red blood cells (SRBC) were used as antigens to investigate the in vivo dose- and time-dependent effects of procarbazine (PCZ) treatment on antibody responses of adult male DBA/2 mice. The mice were exposed to different doses of PCZ (100, 300, and 600 mg/kg) and then immunized with LPS or SRBC at days 0, 7, 14, and 21. Procarbazine treatment had essentially no effect on the number of LPS antibody-producing cells in spleens of mice in the entire range of PCZ dose and time, while the circulating antibody to LPS in serum diminished in mice treated with 600 mg/kg dose. In contrast, PCZ treatment altered the plaque-forming cell (PFC) response of the mice to T-cell dependent antigen SRBC. At 100 mg/kg dose, a slight stimulation of immune response was noticed. However, at higher doses (300 and 600 mg/kg), the number of antibody-producing cells to SRBC was decreased. This decrease was 87% at the highest dose compared to the untreated mice. Besides the antibody-producing cells in spleen, the antibody titer to SRBC in serum was also significantly diminished. This markedly reduced immune response, however, was released with the passage of time and was almost completely recovered by day 21 after the PCZ treatment of the mice. In addition, a very significant decrease in the number of cells per spleen was observed at 600 mg dose. It is suggested that PCZ exerts its immunosuppressive effects by essentially affecting T cells, both by decreasing the antibody synthesis as well as the number of cells.
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PMID:Alterations of immune response of DBA/2 mice by procarbazine treatment. 701 58

In the present study, mice each given a single intraperitoneal injection of Escherichia coli lipopolysaccharide (LPS) responded with increased serum levels of the major envelope glycoprotein, gp70, of endogenous retrovirus. Concentrations of gp70 in their sera began to increase 4 hr after LPS injection, reached maximal 5- to 15-fold increases after 12--24 hr, and returned to the preinjection levels within 3 days. This response occurred only in the strains characterized by high base line levels of serum gp70 (greater than 10 micrograms/ml) such as NZB, NZB X NZW F1, BXSB, MRL, NZW, DBA/2, LG, 129(GIX+), and C57BL/6(GIX+). However, strains such as DBA/1, C3H/St, BALB/c, C57BL/6(GIX-), and 129(GIX-) with lower base line levels of serum gp70 (less than 5 micrograms/ml) made little or no response. This serum gp70 induced by LPS was structurally similar to the gp70 of NZB xenotropic virus that is dominantly expressed in sera from virtually all strains of mice. However, (i) the induced gp70 was virion-free; (ii) xenotropic virus was not isolatable from BXSB, MRL/1, or 129(GIX+) mice injected with LPS; and (iii) amounts of the major structural viral protein, p30, did not increase correspondingly in sera. All of these findings indicate that the increased expression of serum xenotropic viral gp70 in response to LPS did not result from activation of replication-competent xenotropic virus. In addition, the serum gp70 response to LPS was abolished by simultaneous inoculation of an inhibitor of protein synthesis, D-galactosamine. These results strongly suggest that LPS selectively stimulates synthesis of the env gene product, gp70, of NZB xenotropic virus but other viral gene products.
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PMID:Induction of high serum levels of retroviral env gene products (gp70) in mice by bacterial lipopolysaccharide. 702 59


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