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)

Plaque-forming cell responses against sheep erythrocytes, Escherichia coli lipopolysaccharide, pneumococcal polysaccharide, and polyvinylpyrrolidone were examined in mice infected with lymphocytic choriomeningitis virus. A 92 to 96 percent reduction of the thymus-dependent anti-sheep erythrocyte responses was observed 2 to 4 weeks after infection. However, the thymus-independent responses against the three other antigens were close to normal at all stages of the infetion. Studies on allograft immunity of infected C3H mice against DBA/2 mastocytoma cells revealed a severe suppression of the T cell-mediated cytotoxic response which was temporally related to the impaired humoral responsiveness against sheep erythrocytes. The capacity of spleen cells from infected mice to restore immune responsiveness of lethally irradiated recipients against sheep erythrocytes was significantly reduced. The adoptive responses, however, were clearly improved when normal thymus cells were added to the inferior spleen cells. Moreover, it appeared that the spleen cells from immunosuppressed donor mice could not confer suppression to normal lymphoid cells. The presented findings are consistent with the assumption that a numeric deficiency of T cells, or cells belonging to some T cell subpopulation, is the primary cause of lymphocytic choriomeningitis virus-induced immunosuppression.
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PMID:T lymphocyte function as the principal target of lymphocytic choriomeningitis virus-induced immunosuppression. 23 88

We studied functional and immunohistochemical characteristics of cultured rat microglia. Unstimulated microglia did not proliferate. Microglia stimulated with LCM (L929 conditioned medium: colony stimulating factor-1) had proliferative activity and increased acid phosphatase activity. LPS (lipopolysaccharide) and IFN gamma (interferon-gamma) but did not affect proliferative activity. Immunohistochemically, RCA-1 lectin and GS-1 lectin, which react to beta-D-galactose and alpha-D-galactose respectively, strongly reacted to the cytoplasm and membrane of unstimulated microglia. After stimulation with LCM, microglia elongated processes and decreased response to these lectins. On the other hand, microglia stimulated with LCM showed increased reactivity to monoclonal antibody of vimentin. Microglia stimulated with LPS had round shape and had response to these lectins and vimentin. Microglia stimulated with IFN gamma had adhesive activity and weakly stained with these lectins but not with vimentin. ED-1 (monoclonal antibody of rat monocytes/macrophages) reacted to unstimulated and stimulated microglia. In flow cytometry, unstimulated microglia expressed OX-18 (MHC class I) and W3/25 (CD4) antigen. After stimulation with IFN gamma, microglia were induced to express these antigens. CD4 antigen is a marker of helper/inducer T cells and thought to be a receptor of HIV. The results that microglia had CD4 antigen which was further induced with IFN gamma are important to investigate infection of the CNS with HIV. OX-6 (Ia) antigen was induced with IFN gamma. This indicates that the microglia plays a central role in the CNS immune reaction. These characteristics of cultured rat microglia provide useful informations to investigate the pathogenesis of the CNS disorders.
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PMID:[Functional and immunohistochemical studies of cultured rat microglia]. 206 Feb 34

Infection of mice with lymphocytic choriomeningitis virus (LCMV) produces a rapidly induced immuno-suppression manifested by low lymphocyte proliferation in response to lipopolysaccharide (LPS) and concanavalin A (ConA). Analysis of the mechanisms underlying the unresponsiveness to these mitogens was undertaken at the cellular and molecular levels 7 days after infection. The selective elimination of CD8+ T cells and the results of coculture experiments demonstrated that unresponsiveness was not due to suppressor cells. Similarly, the role of inhibitory factors such as prostaglandins was excluded, since indomethacin, which inhibits their production, did not reverse the unresponsiveness. Analysis of different cytokines secreted by ConA-activated macrophages or T cells revealed that interleukin-1 (IL-1), synthesized during the T-dependent activation of macrophages by ConA, was normally produced by cells from LCMV-infected mice. In contrast, IL-2, which is produced by activated CD4+ T cells, was undetectable. Addition of exogenous IL-2 did not restore the proliferative response, although the p55-kilodalton protein of the IL-2 receptor was induced by ConA on CD4+ cells from LCMV-infected mice. Our results can be interpreted as showing that (i) unresponsiveness to mitogens of cells from LCMV-infected mice is not due to altered functions of the macrophages with respect to IL-1 production; (ii) CD4+ cells are activated, since the p55 chain of the IL-2 receptor is induced; (iii) the lack of IL-2 production cannot explain T-cell unresponsiveness, since addition of exogenous IL-2 did not restore the proliferative response. Taken together, these data suggest that T-lymphocyte unresponsiveness should be related to an inherent proliferative defect subsequent to T-cell activation and IL-2 receptor expression.
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PMID:Lymphocytic choriomeningitis virus-induced immunodepression: inherent defect of B and T lymphocytes. 214 39

Peritoneal macrophages elicited by Lactobacillus casei YIT9018 (LCEPM) were incubated in culture for 18 h with L. casei; the culture supernatant (LCM) was then harvested and tested for its ability to increase the cytostatic activity of resident peritoneal macrophages (RPM) and LCEPM. Treatment of RPM with LCM induced activation of macrophages to a cytostatic state against L929, Colon 26, P815, P388D1 and L1210 cells. A combination of recombinant human tumor necrosis factor (rhTNF), recombinant mouse TNF (rmTNF), recombinant human interleukin-1 (rhIL-1) or bacterial lipopolysaccharide with recombinant mouse interferon gamma (rmIFN-gamma) resulted in the synergistic induction of cytostatic activity in RPM. Recombinant mouse granulocyte-macrophage colony-stimulating factor (rmGM-CSF) plus rhTNF increased the cytostatic activity of RPM a little but rmGM-CSF or rhTNF combined with rhIL-1 or alone had no effect. The effect of LCM on RPM was not inhibited by polymyxin B, anti-mTNF antiserum or below 20 U/ml monoclonal anti-rmIFN-gamma antibody (anti-rmIFN-gamma) but was inhibited by more than 40 U/ml anti-rmIFN-gamma, and LCM did not have any interferon antiviral activity. These results suggest that the cytostatic activity of RPM was augmented by the LCM, and that the effect of the LCM may be not due to IFN-gamma, TNF, GM-CSF, IL-1 or a small amount of contaminating lipopolysaccharide.
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PMID:Role of culture supernatant of cytotoxic/cytostatic macrophages in activation of murine resident peritoneal macrophages. 249 78

The role of antibody in immune recovery from infection with lymphocytic choriomeningitis virus (LCMV) strain WE was evaluated in B-cell-depleted mice. Mice were treated from birth with either affinity-purified rabbit anti-mouse immunoglobulin M (IgM), normal rabbit immunoglobulin, or, alternatively, an affinity-purified monoclonal rat anti-mouse IgM antibody (LO-MM-9); untreated mice served as controls. B-cell depletion was considered complete in specifically treated mice according to the following criteria: absence of a significant response to the B-cell mitogen lipopolysaccharide, absence of B cells expressing immunoglobulin on their surfaces, absence of detectable IgM or IgG in serum, and presence in the serum of free anti-IgM antibodies. In organs of mu-suppressed BALB/c mice, LCMV-WE replicated, dependent upon organ, at the same rate or more rapidly and, in general, to higher titers than in normal rabbit immunoglobulin-treated mice; untreated mice eliminated the virus most rapidly and showed lower virus titers. In addition, LCMV-primed control mice cleared a second LCMV challenge very rapidly and contained no virus by day 3, whereas mu-suppressed mice had virus in their blood and organs (except the spleen) up to days 3 to 6. The observed effects of anti-mu treatment may reflect the action of neutralizing antibodies (which so far have been difficult to demonstrate in vivo) or other antibody-dependent antiviral mechanisms which, together with T cells, efficiently control LCMV clearance.
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PMID:Clearance of lymphocytic choriomeningitis virus in antibody- and B-cell-deprived mice. 325 41

The in vivo effect of Nocardia rubra cell-wall skeleton (N-CWS) was studies on the generation of bone marrow granulocyte-macrophage progenitor cells [colony-forming units culture (CFU-c)] and on the levels of myeloid colony-stimulating activity (CSA) in the conditioned medium of the lung (LCM) and serum obtained from mice. In vitro bone marrow culture showed that intraperitoneal (ip) treatment of mice with N-CWS markedly enhanced CFU-c formation induced by stimuli in LCM or serum derived from lipopolysaccharide (LPS)-treated mice. The LCM and serum of mice injected with N-CWS ip were also prepared and assayed for CSA. CSA levels with N-CWS-LCM as well as LPS-LCM used as the standard CSA were markedly greater than those achieved with control LCM. N-CWS-serum also showed a low but significant level of CSA. The CSA level of N-CWS-LCM was maximal at 3 to 5 days after N-CWS injection. These results raise the possibility that enhanced CSA production might be a major mechanism for N-CWS stimulation of granulocyte-macrophage production.
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PMID:Effect of Nocardia rubra cell-wall skeleton on colony-stimulating activity and myeloid colony formation. 712 5

The secretory (tumor necrosis factor, TNF-alpha; nitrite) and cellular response (mitochondrial respiration, TNF-alpha-independent tumoricidal activity) of a pure, lymphocyte-free population of resting, unprimed rat bone marrow-derived mononuclear phagocytes (BMM phi) to direct interaction with viruses, protozoa, and fungi was assessed and compared with that triggered by bacterial agents and interferon-gamma (IFN-gamma). Viruses (herpes simplex, vaccinia, poliomyelitis, vesicular stomatitis, lymphocytic choriomeningitis, Sendai), protozoa (Trypanosoma brucei, Giardia lamblia), and fungi (Penicillium, Trichosporon, Fusarium, Rhizopus, Aspergillus, Geotrichum species) affected primarily the secretion of TNF-alpha and mitochondrial respiration of BMM phi; their effects on the secretion of nitrite and on tumoricidal activity were at best marginal. Collectively, the macrophage response to viruses, protozoa, and fungi was less varied and less marked than that to bacterial agents (intact organisms, peptidoglycan, lipoteichoic acid, lipopolysaccharide) and IFN-gamma.
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PMID:Macrophage response to viruses, protozoa, and fungi: secretory and cellular activities induced in resting unprimed bone marrow-derived mononuclear phagocytes. 799 64

The human monocytic cell line THP-1 was used as a model to study the mechanism of infection in the monocyte/macrophage, a natural target of lymphocytic choriomeningitis virus (LCMV) infection in vivo. Both the virulent strain, LCMV.WE, and the avirulent strain, LCMV.ARM, infected THP-1 cells, but did not stimulate THP-1 cells to secrete interleukin 1 (IL-1) or tumour necrosis factor (TNF-alpha). When lipopolysaccharide (LPS) was added to THP-1 cells together with LCMV, an 80 to 90% reduction in the number of infected cells (measured by immunofluorescence) and a 90% reduction in viral plaques was observed 5 to 6 days post-infection. Neither interferon alpha (IFN-alpha) nor IFN-beta were detected in supernatants from THP-1 cells after the addition of LCMV, LPS, or LPS plus LCMV. In contrast, the same levels of IL-1 and TNF-alpha were observed in the presence of LPS and LCMV, or LPS alone. However, antibodies to IL-1, TNF-alpha, interleukin 6 and IFN-alpha did not block the antiviral effect of LPS. In kinetic studies, LPS added 1 day after adding LCMV to THP-1 cells was still effective in reducing the number of infected cells. Our findings suggest that LPS alters cellular metabolism, possibly through the induction of IFN-alpha, and that IFN-alpha in the absence of LPS suppresses virus production.
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PMID:Lipopolysaccharide inhibits the production of lymphocytic choriomeningitis virus in a human monocytic cell line. 834 56

To investigate the roles of tumor necrosis factor (TNF) and lymphotoxin (LT)-alpha in the development and function of the immune system, the Tnf and Ltalpha genes were simultaneously inactivated in mice by homologous recombination. These mutant mice are highly susceptible to Listeria monocytogenes infection and resistant to endotoxic shock induced by the combined administration of D-galactosamine (D-GaIN) and lipopolysaccharide (LPS). Their splenic microarchitecture is disorganized, characterized by the loss of the clearly defined marginal zone, ill defined T and B cell areas, and absence of MAdCAM-1 and reduced ICAM-1, VCAM-1 and Mac-1 expression. They are devoid of peripheral lymph nodes and Peyer's patches, and show a strong reduction of IgA+ plasma cells in the intestinal lamina propria. The alymphoplasia is accompanied by a marked B lymphocytosis and reduced basal lg levels. Ig depositions in the renal glomerulus and a strong up-regulation of MHC class I antigen expression on endothelial cells of different tissues are observed. The primary humoral immune response towards sheep red blood cells reveals a defective IgG isotype switch, while that against vesicular stomatitis virus is normal. The cytotoxic T cell responses are attenuated, although still effective, against vaccinia, lymphocytic choriomeningitis virus (LCMV-ARM) and LCMV-WE. In conclusion, the combined inactivation of Tnf and Ltalpha confirms their essential role in the normal development and function of the immune system.
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PMID:Multiple immune abnormalities in tumor necrosis factor and lymphotoxin-alpha double-deficient mice. 867 86

Interferon (IFN)-alpha/beta-mediated negative regulation of interleukin 12 (IL-12) and IFN-gamma proteins is reported here. Both IFN-alpha and IFN-beta inhibited fixed Staphylococcus aureus Cowan strain induction of IL-12 and IFN-gamma production by mouse splenic leukocytes in culture. Extended studies with IFN-alpha demonstrated that inhibition was at the level of biologically active IL-12 p70. Effects were selective, as induction of tumor necrosis factor was unaffected and induction of IL-6 was enhanced. Neutralization of IFN-alpha/beta expressed endogenously during infections with murine cytomegalovirus (MCMV) enhanced early IL-12 and IFN-gamma protein production. Furthermore, during infections of mice with lymphocytic choriomeningitis virus (LCMV), this treatment revealed a previously undetected early IL-12 and IFN-gamma protein expression, and mice deficient in IFN-alpha/beta receptor function, but not control mice, also expressed endogenous LCMV-induced IL-12. The effects of IFN-alpha/beta neutralization on production of IL-12 and IFN-gamma during the viral infections were detected in both serum samples and medium conditioned with splenic leukocytes isolated from infected animals. In vitro studies demonstrated that splenic leukocytes isolated from LCMV-infected mice were primed to produce IL-12 in response to stimulation with Staphylococcus aureus Cowan strain, but that this responsiveness was sensitive to added IFN-alpha. Moreover, endogenous IFN-alpha/beta induced by LCMV inhibited in vivo lipopolysaccharide stimulation of IL-12 production. These results demonstrate a new pathway for regulating cytokine responses, and suggest a mechanism for inhibition of IL-12-dependent immune responses during viral infections.
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PMID:Interferon-alpha/beta inhibition of interleukin 12 and interferon-gamma production in vitro and endogenously during viral infection. 901 36


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