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)

Peritoneal and bone marrow-derived macrophages of the C57BL/6 and DBA/2 mouse strains were exposed in vitro to increasing concentrations of the bacterial lysate Broncho-Vaxom (BV), in the presence or absence of macrophage-activating factor (MAF)-rich media. Two metabolic pathways and two functional activities of the macrophages were studied. First, oxidative metabolism was found to increase sharply in macrophages incubated with BV, as measured by the catabolism of glucose via the hexose monophosphate shunt pathway, and by the production of the superoxide anion (O2-). Both effects were further increased by co-stimulation of macrophages with MAF. Second, exposure to BV together with MAF (or with recombinant murine interferon-gamma) led to acquisition by macrophages of the capacity to destroy the intracellular parasite Leishmania enriettii; such activated macrophages were also lytic towards P815 mastocytoma indicator target cells. These cytotoxic properties failed to develop in the absence of MAF. The BV-dependent increase in metabolic and functional activities was of the same magnitude as that induced by incubation of macrophages with 10 ng/ml of bacterial lipopolysaccharide (LPS). Residual contamination of BV by endotoxin was however much lower. In addition, polymyxin B, a LPS inhibitor, blocked the effect of LPS without significantly affecting macrophage stimulation by BV. These experiments indicate that BV can markedly stimulate macrophage metabolic and functional parameters that are important for host defense against pathogens and tumors.
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PMID:Stimulation by a bacterial extract (Broncho-Vaxom) of the metabolic and functional activities of murine macrophages. 255 25

T-cell clones were derived from autoimmune prone (NZB) and non-autoimmune (C58) strains of mice and tested for their effects in several assays of B-cell responsiveness. Clones from the C58 strain suppressed lipopolysaccharide LPS-stimulated B-cell proliferation, activation and immunoglobulin synthesis. In contrast, an NZB-derived clone enhanced these measures of B-cell response. The effects of the NZB clone were more notable on splenic target populations taken from mice 6 months of age or older. MHC-compatible DBA/2 spleen cells also showed enhancement of B-cell activation, but not of immunoglobulin synthesis by the NZB clone. It has been shown previously that all of the clones suppress T-cell proliferative responses. A potentially important skewing of the immune system toward humoral rather than cellular responses is therefore mediated by this clone derived from an autoimmune strain.
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PMID:Immunoregulatory effects of cloned T cells on B-cell responses: comparison of autoimmune and non-autoimmune derived clones. 256 83

The present study investigates the cellular and molecular mechanisms responsible for expressing genetic control of type II collagen-induced murine chronic arthritis. Analyses were made for both humoral and cellular immune responses, since the induction of arthritis required synergy between both types of immunities. Immunization of high (DBA/1) and low (C57BL/6, C3H/He, BALB/c) responder mice with native bovine type II collagen resulted in the production of the respective high and low levels of anti-collagen antibody. However, polyclonal in vitro stimulation of normal spleen cells from high or low responder mice with lipopolysaccharide (LPS) induced a comparable magnitude of anti-collagen antibody responses, indicating the localization of the genetic defect at cellular levels other than B cells themselves. In contrast to immunization with native collagen, sensitization of DBA/1 mice with heat-denatured collagen failed to stimulate B cells, but resulted in selective generation of L3T4+ T cell-mediated immunity. These included anti-collagen delayed-type-hypersensitivity (DTH) responses and the generation of various interleukins (IL) responsible for antibody production as well as DTH responses. It was demonstrated that there was appreciable difference in the magnitudes of these responses between lymphoid cells from high and low responder mice. Differential effects of sensitization with heat-denatured collagen in high versus low responders were reflected on the genetic difference in the development of chronic arthritis. A typical arthritis was induced neither in denatured collagen-sensitized DBA/1 mice nor in unsensitized mice transferred with anti-collagen antiserum. However, the antiserum transfer into denatured collagen-sensitized DBA/1 mice induced chronic perpetuating arthritis. This sharply contrasted with the failure of the same aliquot of the antiserum to induce a chronic arthritis when inoculated into denatured collagen-sensitized low responder mice. These results indicate that the genetic control of the induction of arthritis is expressed on L3T4+ T cells which are required for generating anti-collagen humoral as well as cell-mediated immunities as assessed by DTH responses in vivo or lymphokine productions in vitro.
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PMID:Type II collagen-induced murine arthritis. II. Genetic control of arthritis induction is expressed on L3T4+ T cells required for humoral as well as cell-mediated immune responses to type II collagen. 257 23

The hepatoprotective effect of Gomisin A (TJN-101), which is a lignan compound isolated from Schizandra fruits, was studied on three immunologic liver injury models in mice. The first liver injury model was produced by the injection of anti-basic liver protein (BLP) antibody into DBA/2 mice which had been previously immunized with rabbit IgG (RGG). Other models were effected by injection of anti-liver specific protein (LSP) antibody into DBA/2 mice or by the injection of bacterial lipopolysaccharide (LPS) into ddY mice pretreated with Corynebacterium parvum (C. parvum). TJN-101 inhibited the elevation of transaminase (GOT and GPT) activities and showed the tendency to inhibit the histopathological changes of the liver in all models. Moreover, TJN-101 inhibited deoxycholic acid-induced release of transaminase from cultured rat hepatocytes in vitro, but did not affect the formation of hemolytic plaque forming cells in immunized mice spleens and hemolytic activity of guinea pig complement in immunohemolysis reaction. These results, therefore, suggested that the hepatoprotective effect of TJN-101 could be related to the protecting effect of hepatocyte plasma membrane rather than the inhibiting effects of the antibody formation and complement activity.
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PMID:The effect of gomisin A on immunologic liver injury in mice. 271 84

The induction of sister chromatid exchange (SCE) by N-methyl-N-nitrosourea (MNU) was studied in spleen and thymus lymphocytes from AKR mice, which are highly susceptible to MNU-produced thymomas, CBA mice, which are much less sensitive to induction of thymomas by MNU, and C57BL/6N x DBA/2J F1 mice. MNU produced dose-related increases in SCE in concanavalin A (Con A)- and lipopolysaccharide-stimulated spleen lymphocytes and Con A-stimulated thymus lymphocytes from each mouse strain at 1 and 24 h posttreatment. MNU-induced SCE were generally higher in Con A-stimulated spleen lymphocytes compared to lipopolysaccharide-stimulated spleen lymphocytes and Con A-stimulated thymus lymphocytes from each mouse strain. On the whole, MNU-produced SCE were lower in AKR and CBA spleens than in C57BL/6N x DBA/2J F1 spleens. In addition, MNU-induced SCE levels in thymus lymphocytes from all three strains of mice were, for the most part, similar. These results indicate that if differences in MNU-induced genotoxicity in AKR, CBA, and C57BL/6N x DBA/2J F1 thymus lymphocytes exist, these differences cannot be ascertained by use of the in vivo/in vitro SCE assay.
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PMID:Comparison of sister chromatid exchanges in spleen and thymus lymphocytes from AKR, C57BL/6N x DBA/2J F1, and CBA mice following in vivo exposure to N-methyl-N-nitrosourea. 278 6

The spontaneous in vitro anti-DNA antibody response generated by preautoimmune and many normal mouse spleen cells was suppressed by the addition of syngeneic thymocytes or splenic T cells. Suppressive activity was found in normal mice (DBA/2J) and to an equivalent degree in the autoimmune (New Zealand Black X New Zealand White)F1 (B/W) strain. The suppressor cells were cortisone-resistant, radiosensitive and carried Lyt 1 and Lyt 2 markers. Nonspecific suppression was not involved since the primary and primed in vitro anti-sheep erythrocyte (anti-SRBC) responses were unaffected. Both spontaneous and lipopolysaccharide-stimulated anti-DNA antibody responses could be suppressed. There was no difference in the suppressive activity of cells from young or old, normal or autoimmune mice. These T cells may therefore play a role in preventing the anti-DNA antibody response in normal and young B/W mice, but evidently fail to influence the development of in vivo anti-DNA autoimmune responses in the old B/W mice.
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PMID:Regulation of an in vitro anti-DNA antibody response by thymocytes and T cells from NZB/W and normal mice. 286 Sep 75

L-leucyl-L-leucine methyl ester (Leu-Leu-OMe) is selectively toxic for human natural killer (NK) cells and cytotoxic T lymphocytes (CTL) at both the precursor and effector stage of differentiation. The present studies explored the effects of Leu-Leu-OMe on murine spleen cell function. Leu-Leu-OMe exposure removed NK function from murine spleen cells but spared their capacity to proliferate in response to lipopolysaccharide and Con A. The capacity to generate CTL from both L3T4 (+) and Lyt-2 (+) precursors was lost after Leu-Leu-OMe treatment, whereas alloantigen-induced proliferation and interleukin 2 (IL 2) production by L3T4 (+) T helper cells remained intact. Lethal graft vs host disease (GVHD), which developed in irradiated (C57BL/6 X DBA/2)F1 recipients of C57BL/6 bone marrow and spleen cells was completely prevented by Leu-Leu-OMe treatment of donor cells. In contrast depletion of Lyt-2 positive cells from the donor inoculum did not prevent acute GVHD in this fully major histo-compatibility complex (MHC) incompatible strain combination. However, Leu-Leu-OMe treatment of the Lyt-2 depleted inoculum completely prevented lethal GVHD, although the treated cells retained the capacity to proliferate and secrete IL 2 normally after in vitro stimulation with (C57BL/6 X DFA/2)F1 spleen cells. These findings indicate that L3T4 (+) T helper cells alone are unable to initiate lethal GVHD in this H-2 incompatible strain combination. Rather, lethal GVHD requires the transfer of a Leu-Leu-OMe sensitive T cell subset, likely to be thymus educated pre-CTL. Leu-Leu-OMe treatment should provide a useful way to delineate subpopulations of cells involved in the production of lethal GVHD and an approach to preventing this complication of bone marrow transplantation.
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PMID:Lethal graft-vs-host disease across major histocompatibility barriers: requirement for leucyl-leucine methyl ester sensitive cytotoxic T cells. 294 80

A test system that allows a precise monitoring of intracellular killing of Leishmania parasites was used to measure the leishmanicidal capacity of activated macrophages from different strains of mice. Activation was obtained by exposure to dilutions of lymphokine (LK)-rich medium in the presence of ng/ml amounts of E. coli lipopolysaccharide (LPS). Highest leishmanicidal activity was displayed by macrophages from the healer mouse strain CBA/T6, whereas cells from the nonhealer strains DBA/2 and BALB/c were less effective. C3H/HeJ macrophages from a healer but LPS-unresponsive mouse strain failed to destroy leishmanias under these conditions. Experiments were then performed to determine the level of respiratory burst activity in the various macrophage populations. Hexose monophosphate shunt stimulation was higher in CBA/T6 than in BALB/c or DBA/2 macrophages, and only marginal in C3H/HeJ cells, correlating with differing leishmanicidal activities of such macrophages under the present experimental conditions. Measurements of O2- and H2O2 secretion and of chemiluminescence led to similar findings, i.e., CBA/T6 macrophages released higher amounts of oxygen metabolites than BALB/c cells activated under the same conditions, whereas C3H/HeJ cells were the least active. The results obtained by the four assays of oxidative metabolism were consistent in that endotoxin itself (in the 10 to 30 ng/ml range) stimulated the oxidative response of macrophages to a level close to that achieved by using LPS and LK together, however, only in the latter situation were parasites destroyed.
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PMID:Correlation between enhanced oxidative metabolism and leishmanicidal activity in activated macrophages from healer and nonhealer mouse strains. 300 12

Three synthetic glycolipids, maltose tetrapalmitate (MTP), maltose hexastearate (MHS), and maltose hexalinoleate (MHL) prepared as nontoxic lipid A analogs, and Escherichia coli lipopolysaccharide (LPS) were assayed for their mitogenic activity using spleen lymphocytes in nine inbred mouse strains and three F1 hybrids. The MTP and LPS were also assayed for their ability to enhance plaque-forming cell (PFC) responses using sheep red blood cells as the antigen in the same inbred mouse strains and F1 hybrids, The mitogenic activity of synthetic glyco-lipids was several fold lower than that of LPS and MHL was inferior to MTP and MHS. DBA/2J was the most responsive strain for MTP and DBA/1J and C3H/HeJ the least. The mitogenic activity of MTP was generally in agreement with the PFC response stimulation by it. Low-dose cyclophosphamide treatment of mice synergized MTP for PFC response augmentation. Genetic studies on MTP mitogenicity revealed that 90% of responder DBA/2J X nonresponder C3H/HeJ F1 hybrids had intermediate mitogenic activity. Among F2, 73% had intermediate-high activity and 27% were nonmitogenic. Among F1 X C3H/HeJ backcrosses 11% had high, 56% intermediate, and 33% had no mitogenic activity, whereas, for the F1 X DBA/2J backcross, 14% had high, 36% intermediate, and 50% low or negligible activity. The data favored a single gene for MTP activation of immune cells.
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PMID:Mitogenic, immunoadjuvancy, and genetic studies on fatty acyl maltose. 305 44

Recent reports suggest that the immunotoxicity of certain polycyclic aromatic hydrocarbons is associated with the Ah locus in mice. To test whether immunosuppression mediated by 7,12-dimethylbenz[a]anthracene (DMBA) is regulated by the Ah locus, several endpoints of immune function were measured in Ah-responsive B6C3F1 and Ah-nonresponsive DBA/2N and in Ah-congenic C57BL/6J (responsive B6-AhbAhd and nonresponsive B6-AhdAhd) mice dosed sc with up to 100 micrograms/g DMBA in corn oil. Some groups of B6C3F1 and DBA/2N mice were exposed to 100 micrograms/g benzo[a]pyrene (B(a)P) or 1 nmol 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for determination of hepatic microsomal monooxygenase activity. The body weights of all mice were unaffected by DMBA exposure, but thymus weights and spleen cellularity were decreased. Antibody plaque-forming cells (PFC) measured 4 days after iv sheep erythrocyte (SRBC) immunization were suppressed 99% in B6C3F1 and 96% in DBA/2 mice. Antibody PFC after in vitro immunization to SRBC were similarly suppressed 98% in both B6-AhbAhd and B6-AhdAhd Ah-congenic mice exposed to 100 micrograms/g DMBA. Responses to the T-cell mitogens concanavalin A and phytohemagglutinin were significantly suppressed in both B6C3F1 and DBA/2N strains, as was mitogenesis to bacterial lipopolysaccharide. The unidirectional mixed lymphocyte responses of the congenic strains were suppressed 76% in B6-AhbAhd and 85% in B6-AhdAhd, cytotoxic lymphocyte generation was suppressed 68% in B6-AhbAhd and 78% in B6-AhdAhd. The overall differences between immunosuppressive responses in splenocytes from B6-AhbAhd and B6-AhdAhd congenics were not significant. Induction of cytochrome P1-450, a marker of Ah responsiveness, was determined by 7-ethoxycoumarin O-deethylase monooxygenase activity in hepatic microsomes or splenocytes. This monooxygenase activity was not significantly increased in either B6C3F1 or DBA/2 mice exposed to DMBA, whereas B(a)P and TCDD exposure significantly induced enzyme activity in B6C3F1 hepatocytes. These data suggest that DMBA has an immunosuppressive action on murine splenocytes which is independent of the Ah locus and associated induction of cytochrome P1-450 xenobiotic-metabolizing enzymes.
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PMID:Immunosuppression following exposure to 7,12-dimethylbenz[a]anthracene (DMBA) in Ah-responsive and Ah-nonresponsive mice. 312 68


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