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)

Resistance to mouse hepatitis virus (MHV) in C3H mice is a genetic trait which appears 3-4 weeks after birth. However, when these animals were weaned on a low protein diet (8% casein), they remained susceptible to MHV-2 infection until they reached 8-9 weeks of age. During this period, the protein-restricted C3H mice were as susceptible to MHV-2 as the genetically susceptible congenic C3Hss strain. The delay in the emergence of resistance in the protein-restricted mice could be corrected by injecting these animals with spleen cells from 6-week-old C3H mice. Thymocytes from normal C3H mice, and splenocytes and thymocytes from protein-restricted C3H mice, were not protective. However, spleen cells from the protein-restricted mice were more responsive to phytohaemagglutinin, lipopolysaccharide and concanavalin A than spleen cells from normal C3H. The enhanced lymphoproliferative response in spleen cells from protein-restricted mice was abrogated by the addition of plastic-adherent cells obtained from normal C3H spleens. Spleen cells from protein-restricted and from genetically susceptible C3Hss mice also possessed more spontaneous cytotoxicity against MHV-infected 3T3 fibroblasts.
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PMID:Influences of nutrition on immunity and susceptibility to mouse hepatitis virus type 2. 299 Nov 26

Infection of mice with Mycobacterium bovis BCG sensitizes them for immune induction of interferon (IFN)-gamma by specific antigen. These mice were found also to respond to lipopolysaccharide (LPS) and concanavalin A (Con A) with high level production of IFN-gamma in the circulation, which was not observed in control mice. In this study, we compared the IFN-gamma response to LPS with that to Con A in an attempt to clarify the cellular mechanisms responsible for in vivo LPS-induced IFN-gamma production. Consequently, (i) the responses to LPS and Con A differed in the kinetics, that to LPS having a longer lag period. (ii) Spleen cells taken from infected mice produced little IFN-gamma in response to LPS, but they showed a higher IFN-gamma response to Con A than those from control mice. (iii) By treating infected mice with immunosuppressive drugs or antibodies to T and natural killer cells before challenge with the inducers, it was indicated that different cellular systems are involved in the IFN-gamma responses to LPS and to Con A.
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PMID:Cellular mechanisms in in vivo production of gamma interferon induced by lipopolysaccharide in mice infected with Mycobacterium bovis BCG. 299 37

Splenocytes from 25 patients with severe hepatosplenic schistosomiasis mansoni were obtained after therapeutic splenectomy. Spleen cells were phenotyped and analysed for responsiveness to mitogens or heterogeneous schistosome-derived antigenic preparations (eggs, SEA; adult worms, SWAP; cercariae, CERC) in blastogenesis assays and lymphokine production systems, and were compared with peripheral blood mononuclear cells (PBMN). Splenic lymphocytes were 55% T lymphocytes (sheep erythrocyte rosette-positive) and 37% surface immunoglobulin-positive B lymphocytes. The mean T4+:T8+ ratio of these splenocytes was 1.0. Phytohaemagglutinin stimulated spleen cell production of the lymphokine mitogenic factor, but exposure to SEA or SWAP did not. Spleen cell and PBMN blastogenic responses to SEA and SWAP were sometimes, but not always in accord. Removal of plastic adherent cells allowed the non-adherent spleen cells of 30-40% of the patients to respond substantially more vigorously to SEA, SWAP and CERC. Spleen cells from a subgroup of 20-30% of the patients failed to respond to the schistosomal antigens regardless of removal of adherent cells. Spleen cell responses to gram-negative lipopolysaccharide peaked on day 5 or 6 of culture, and were augmented by adherent cell removal. Pokeweek mitogen-stimulated responses were optimal on day 5 of culture. Spleen cells from most severe, hepatosplenic schistosomiasis mansoni patients do not respond well to schistosomal antigens or B-cell mitogens. The splenic responses of many of these patients were elevated by the removal of adherent spleen cells.
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PMID:Immune responses during human schistosomiasis mansoni. XIII. Immunological status of spleen cells from hospital patients with hepatosplenic disease. 309 36

The mouse macrophage cell line J774 was easily infected by T. cruzi epimastigotes which were transformed to amastigotes that multiplied inside the cells. Spleen-T-cells from T. cruzi immune mice stimulated with Concanavalin A or T. cruzi, but not with unrelated antigens, released lymphokines into the supernatants that when added to J774 cells were unable to induce complete trypanocidal activity, although they were able to delay the rate of infection by protecting the cells from being infected. Addition of bacterial lipopolysaccharide (LPS), although inactive by itself, acted synergistically with the supernatants in inducing complete trypanocidal activity without affecting the susceptibility of J774 cells to infection. Gamma-interferon (gamma-IFN) activity was detected in the supernatants, however, but was not solely responsible for the trypanocidal inducing activities, since: there was no correlation between the levels of gamma-IFN and macrophage activation; gamma-IFN alone was less effective than the supernatants alone; and two active fractions of 100,000-150,000 mol. wt and 30,000 mol. wt were separated by gel filtration chromatography of the lymphokine preparations. The latter, which showed the characteristics of gamma-IFN with respect to size, pH 2 sensitivity and antiviral activity, had some trypanocidal activity alone. However, the 100,000-150,000 mol. wt fraction was active only in the presence of LPS. Finally, this trypanocidal inducing activity of the supernatants was not due to the induction of synthesis of gamma-IFN by the J774 cells.
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PMID:Activation by synergism between endotoxin and lymphokines of the mouse macrophage cell line J774 against infection by Trypanosoma cruzi. 310 22

The effect of increasing doses of cyclosporin A (CsA) given to mice infected intravenously with Mycobacterium bovis BCG was investigated. Development of both tuberculin hypersensitivity and acquired antituberculous resistance was suppressed in a dose-responsive manner. Daily dosages at 100 mg/kg of body weight prevented any reduction in the BCG counts within the lungs, liver, or spleen. This effect was associated with lowered nonspecific resistance to a Listeria monocytogenes challenge and a decline in specific protective immunity adoptively transferred to naive recipients. CsA treatment had no effect on antilisterial activity by activated macrophages or on the antituberculous immunity expressed by specific memory T cells. CsA treatment inhibited the ability of BCG-vaccinated mice to produce gamma interferon (IFN-gamma) after a secondary stimulation with live BCG or with lipopolysaccharide. Spleen cells from BCG-infected mice which were exposed to daily treatment with CsA showed reduced IFN-gamma production in response to purified protein derivative or concanavalin A stimulation, suggesting that the immunosuppressive effect of CsA on BCG-infected mice was expressed by inhibiting the development of effector T cells responsible for the production of IFN-gamma.
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PMID:Immunosuppressive effect of cyclosporin A on Mycobacterium bovis BCG infections in mice. 311 69

Macrophage synthesis of nitrite and nitrate after activation by BCG infection or by treatment in vitro with both T cell-derived (lymphokines (LK) or recombinant murine interferon-gamma (IFN-gamma] and bacterial (lipopolysaccharide (LPS) and heat-killed bacillus Calmette-Guerin (hk BCG] agents was studied by using macrophages from C3H/He and C3H/HeJ mice. Spleen and peritoneal macrophages isolated from BCG-infected donors that were producing nitrate continued to synthesize nitrite and nitrate in culture. LPS treatment in vitro (25 or 50 micrograms/ml) additionally increased this nitrite/nitrate synthesis. Thioglycolate-elicited macrophages from non-infected C3H/HeJ mice treated with LK also produced nitrite/nitrate, and concurrent LPS (0.1 to 50 micrograms/ml) treatment resulted in enhanced synthesis. Recombinant IFN-gamma also stimulated nitrite/nitrate synthesis by C3H/He and CeH/HeJ macrophages as did LPS (C3H/He only) and hk BCG. When given concurrently with either LPS or hk BCG, IFN-gamma enhanced C3H/He and C3H/HeJ macrophage nitrite/nitrate synthesis over that produced by macrophages treated with either LPS or hk BCG alone. Macrophages activated in vitro exhibited a 4 to 12 hr lag time before engaging in nitrite/nitrate synthesis, which then proceeded for 36 to 42 hr at linear rates. Daily medium renewal did not alter the synthesis kinetics but increased the total amount of nitrite/nitrate produced. Nitrate and nitrite were stable under the conditions of culture and when added did not influence additional macrophage synthesis. Taken together, these results indicate that T cell lymphokines and IFN-gamma are powerful modulators of macrophage nitrite/nitrate synthesis during BCG infection and in vitro, and nitrite/nitrate synthesis appears to be common property of both primed and fully activated macrophage populations.
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PMID:Induction of nitrite/nitrate synthesis in murine macrophages by BCG infection, lymphokines, or interferon-gamma. 311 Feb 73

The subcutaneous growth of EL4 cells was significantly accelerated when they were injected together with spleen cells collected from mice which had received EL4 cells SC 14 days previously, and all mice died within 18 days after receiving this mixture; 80% of mice which received a mixture of EL4 and spleen cells collected immediately after EL4 graft survived over 40 days. Spleen cells collected 14 days after EL4 graft suppressed the blastogenic responses of normal spleen lymphocytes to concanavalin A, pokeweed mitogen, and lipopolysaccharide of Escherichia coli in a mixed culture system. Acceleration of tumor growth was retarded when EL4 cells were injected together with spleen cells from EL4-bearing mice treated with both Salmonella typhimurium mini-cells and mitomycin C, and 60% of mice survived over 40 days. Blastogenic responses of normal spleen lymphocytes mixed with spleen cells from EL4-bearing mice treated with both mini-cells and mitomycin C were restored almost to control levels. The results suggest that combination treatment with mini-cells and mitomycin C synergistically inhibits the induction of suppressor cells in EL4-bearing mice.
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PMID:Synergistic anti-suppressor effect of mini cells prepared from Salmonella typhimurium and mitomycin C in EL 4-bearing mice. 315 37

In vivo exposure of mice to lidocaine (0.25 mg/10 g body weight 4 times a day for 7 days) resulted in impairment of immunocompetent cell function. Spleen lymphocytes removed from animals immediately and 3 days after lidocaine exposure showed changes in their surface charge properties, inhibition of blastogenesis in response to concanavalin A and lipopolysaccharide, and inhibition of antigen-stimulated activation as measured by the mixed lymphocyte reaction. Lymphocytes from animals sensitized to keyhole limpet hemocyanin showed a significantly lower capacity to produce macrophage migration inhibitory factor 8 days after termination of exposure to lidocaine. Animals exposed to the drug were unable to accumulate an adequate number of immunocompetent cells at the site of challenge with a foreign substance (i.e. dextran), and the ability of the animals to destroy tumor cells nonspecifically and specifically was also impaired. The results indicated that chronic exposure to lidocaine resulted in impairment of lymphocyte function, even in the subsequent absence of the drug, and in significant changes in the expression of the immune response.
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PMID:Effect of lidocaine on the function of immunocompetent cells. II. Chronic in vivo exposure and its effects on mouse lymphocyte activation and expression of immunity. 316 Jun 79

Spleen cells from young NZB/NZW mice spontaneously produce IgM antihistone and anti-DNA antibodies in culture, and this in vitro autoantibody production is T-cell dependent. In the present studies, we investigated the response of young autoantibody-producing NZB/NZW B cells to various T-cell-derived signals. Stimulation with unprimed allogeneic T cells resulted in a 10- to 20-fold increase in IgM antihistone and anti-DNA antibody production compared with cultures of B cells alone. The responding cells were found in the large B-cell fraction after separation on Percoll gradients. Allo-stimulated B cells from nonautoimmune mice produced much lower absolute amounts of IgM autoantibodies as well as total IgM compared with NZB/NZW cells. Marked IgM antinuclear antibody and total IgM production was also observed when NZB/NZW B cells were cultured with supernatants from TH2 but not TH1 T-helper clones. Although B cells from nonautoimmune mice produced high levels of autoantibodies after stimulation with lipopolysaccharide, only minimal levels were secreted in response to the active supernatants. These results suggest that young NZB/NZW mice have IgM autoantibody-producing B cells that are more sensitive to certain T-cell-derived signals compared with B cells from normal mice. Although these hyperresponsive NZB/NZW cells appear to be in an advanced stage of activation, they require additional T-cell signals to express this abnormality.
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PMID:Enhanced response of autoantibody-secreting B cells from young NZB/NZW mice to T-cell-derived differentiation signals. 325 28

In order to clarify the mechanism(s) of increased splenic hematopoiesis noted in lipopolysaccharide (LPS)-injected mice, the effects of spleen cell-conditioned medium (SPCM) on megakaryocyte colony (CFU-meg) formation and early erythroid (BFU-e) differentiation were investigated. After spleen cells from LPS-injected mice were incubated for 3 days, the SPCM was assayed for megakaryocyte colony-stimulating factor (Meg-CSF) in CFU-meg assay and for burst-promoting activity (BPA) and erythropoietin (Epo) in erythroid colony assays (i.e., CFU-e, BFU-e). Colony formation of CFU-meg and BFU-e peaked with the addition of 30 and 10-15% SPCM, respectively. Spleen cells from LPS-injected mice produced Meg-CSF and BPA when compared with controls. However, conditioned medium from spleen cells depleted of phagocytic cells had low Meg-CSF and BPA. SPCM did not contain detectable quantities of Epo. It appears likely that local splenic production of Meg-CSF and BPA may affect proliferation of CFU-meg and erythroid progenitor cells in the spleen.
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PMID:Megakaryocyte colony-stimulating factor and burst-promoting activity in LPS-treated mouse spleen cell-conditioned medium. 326 23


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