Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A synthetic muramyldipeptide (MDP) and two analogues, B30-MDP and MDP-Lys(L18), augmented serum interferon (IFN) production in mice by the inducers lipopolysaccharide (LPS) and polyinosinic acid:polycytidylic acid (poly I:C), and also augmented immune IFN production induced by purified protein derivative (PPD) in mycobacteria-sensitized mice. These compounds were most effective when administered to mice one day before the interferon inducer. By contrast, IFN production in mice by either oral tilorone or virus infection was not enhanced with these compounds. Since LPS and poly I:C are well known as early-type IFN inducers, and tilorone and virus infection are late-type inducers, we presume that MDP and its analogues are able to augment only early-type IFN production. This enhancing effect may be mediated by macrophage activation. In vivo antiviral activity of MDP and its analogues was further tested in mice infected with vaccinia virus (VV) using early-type inducers. When mice previously treated with MDP or its analogues were stimulated for IFN production with a low dose of LPS, protective activity against VV infection was markedly enhanced.
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PMID:Enhancement by muramyldipeptides of the activities of early-type inducers of interferon. 241 80

To examine the immunopharmacological actions of an extract isolated from inflamed skin of rabbits inoculated with Vaccinia virus (Neurotropin), its effect on the immune responses in aging BALB/c mice was examined. Neurotropin clearly restored the decreasing T-cell-dependent immune responses such as delayed-type hypersensitivity (DTH) response and plaque-forming cells (PFC) response to sheep red blood cells (SRBC) when administered i.p. from 13 months old (mo) to 16 mo. However, Neurotropin administration from 2 to 5 mo had no effect on the immune responses of young animals. Neurotropin administration from 13 to 16 mo restored not only the T-cell proliferation of spleen cells induced by concanavalin A (Con A) and phytohemagglutinin (PHA), but also the interleukin-2 (IL-2) production by spleen cells activated with Con A. However, Neurotropin did not affect the responsiveness of Con A-activated spleen cells to exogenous recombinant IL-2. An absence of suppressor cells capable of inhibiting the IL-2 production in the spleens was confirmed in the 16 mo mice. Neurotropin administration also restored IL-1 production by peritoneal macrophages stimulated with lipopolysaccharide (LPS). These results suggest that long-term administration of Neurotropin restores the decreasing T-cell-dependent immune responses through the recovery of IL-2 and in part IL-1 production, but not the responsiveness to IL-2 in aging BALB/c mice.
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PMID:Immunopharmacological actions of an extract isolated from inflamed skin of rabbits inoculated with Vaccinia virus (Neurotropin)--II. Restorative effect on immune responses through the recovery of IL-2 production in aging mice. 268 Oct 5

Exposure of hamsters to microwave (MW) energy (2.45 GHz, 25 mW/cm2, 1 h) resulted in activation of peritoneal macrophages (PM) to a viricidal state restricting the replication of vesicular stomatitis virus (VSV). The PM from MW-exposed hamsters were viricidal as early as 1 day after exposure and remained active for 5 days. Immunization of hamsters with vaccinia virus induced viricidal PM by 3 to 4 days and they remained active for 7 days. To test the hypothesis that thermogenic MW exposure results in the release of endotoxin across the intestinal epithelium which subsequently activates PM, hamsters were injected with lipopolysaccharide (LPS) and their viricidal activity was studied. Lipopolysaccharide in vitro (0.2 microgram) and in vivo (0.5 microgram) activated macrophages to a viricidal state. When administered in vivo, LPS (0.5 microgram) activated macrophages as early as 1 day and the activity remained for 3 days. While MW exposure of PM in vitro failed to induce viricidal activity, exposure of PM to LPS in vitro induced strong viricidal activity. This suggests that the in vivo response of PM to MW is an indirect one, which is consistent with the hypothesis that MW-induced PM viricidal activity may be mediated via LPS. In preliminary experiments, MW exposure resulted in extended survival time for hamsters challenged with a lethal dose of vesicular stomatitis virus, supporting the concept that MW-activated PM may be a useful therapeutic modality.
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PMID:Effects of microwave exposure on the hamster immune system. III. Macrophage resistance to vesicular stomatitis virus infection. 609 58

A simian virus 40-transformed mouse macrophage line, BB-W-531-2, was examined for its ability to produce interferon. BB-W-531-2 cells showed a phenotypic change between the macrophage and the nonmacrophage states. A viral inhibitor (interferon) was produced by the cells during the phenotypic change from the nonmacrophage to the macrophage state. Cells having macrophage properties were well capable of producing interferon when they were stimulated with ultraviolet-inactivated vaccinia virus, lipopolysaccharide, a streptococcal preparation (OK-432) or polyinosinate . polycytidylate. In contrast, cells that had lost their macrophage properties did not produce interferon even when they were given the same treatments as the cells having macrophage properties. The results suggest that the ability of BB-W-531-2 cells to produce interferon is associated with the expression of several macrophage properties.
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PMID:Production of interferon by an SV40-transformed macrophage line, BB-W-531-2. 616 94

Neurotropin (NSP) is an extract isolated from vaccinia virus-inoculated and inflamed skin of rabbits. The present study was undertaken to examine the immunostimulating actions of NSP. NSP alone did not induce a proliferation of spleen cells from mice or human peripheral blood lymphocytes (PBL). However, NSP clearly enhanced concanavalin A (Con A)-induced proliferation of both spleen cells and human PBL, but slightly inhibited lipopolysaccharide (LPS)-induced proliferation of spleen cells. NSP reversed the decreases of Con A-induced proliferation of spleen cells pretreated with mitomycin C (MMC) in a dose of 5 microgram/ml or irradiated at 100 to 500 R, while NSP did not reverse the decreases of LPS-induced proliferation of spleen cells pretreated with MMC, in a dose of 5 to 50 microgram/ml, or irradiated at 100 to 1000 R. NSP enhanced in a dose-dependent fashion one-way mixed lymphocytes culture (MLC) reaction using MMC-treated spleen cells from BDF1 mice as stimulator cells and those from C57BL/6 mice as responder cells, respectively. NSP reversed the considerable decrease of MLC-mediated proliferation of responder cells pretreated with MMC, in a dose of 5 to 10 microgram/ml, or irradiated at 100 to 250 R. These results indicate that NSP activates T cell function participating in cell-mediated immunity.
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PMID:[Immunopharmacological actions of neurotropin. (1). Immunostimulating actions of neurotropin (author's transl)]. 732 58

In order to analyse the physiological relevance of the 55 kDa tumor necrosis factor receptor 1 (TNFR1) and its role in various TNF related pathological conditions, such as septic shock, we have generated mice by gene targeting deficient for TNFR1 expression. The TNFR1-deficient mice are unable to cope with Listeria monocytogenes infections but mount an apparently normal immune response when challenged with Vaccinia or LCMV viruses. They are resistant to the lethal effects of lipopolysaccharide (LPS) after sensitization with D-galactosamine (D-GalN) but remain sensitive to very high doses of LPS given alone. We have analyzed functions relevant to inflammatory processes, such as adhesion, secondary factor release, and proliferation in fibroblasts derived from these mice. We show that the TNFR1 virtually monopolises TNF-mediated signaling in all these situations and that the 75 kDa TNFR2 seems to be largely restricted to an accessory role, which is compatible with the previously established "ligand passing" hypothesis.
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PMID:Phenotypic analysis of TNFR1-deficient mice and characterization of TNFR1-deficient fibroblasts in vitro. 774

Interleukin-1 (IL-1) binding found in rodent brain, and its biological effect on astroglial cells, suggests that the receptor for IL-1 alpha may be located on astrocytes. A radioligand receptor assay performed on pure mouse astrocyte cultures revealed the presence of one binding site [type I, molecular weight (MW) 80,000], with Kd = 0.3 x 10(-1) M), at a density of 150 receptors/cell. The specific, saturable and displaceable high-affinity binding took place in a time- and temperature-dependent way. The receptor-IL-1 alpha complex was quickly endocytosed at 37 degrees but not at 4 degrees. The receptor expression was up-regulated by Theiler's virus, interferon-gamma, tumour necrosis factor and IL-6; was not affected by vaccinia virus infection; and decreased after lipopolysaccharide treatment.
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PMID:Demonstration of the presence of an interleukin-1 receptor on the surface of murine astrocytes and its regulation by cytokines and Theiler's virus. 792 86

The complete amino acid sequence of human Growth/differentiation factor 5 (huGdf5), a new member of the TGF-beta superfamily, has been determined through initial degenerate PCR and subsequent cloning and nucleotide sequencing of genomic DNA and cDNA encoding the precursor and flanking regions. The huGdf5 gene consists of only two coding exons. The protein is highly homologous to its murine equivalent, particularly the mature part which differs only by one amino acid. Expression in HuTK- cells using recombinant vaccinia virus revealed the expected processed dimeric mature protein. Antibodies against huGdf5 were raised in chicken.
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PMID:Cloning and expression of recombinant human growth/differentiation factor 5. 798 May 26

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

Interleukin-6 (IL-6) is a multifunctional cytokine that regulates various aspects of the immune response, acute-phase reaction and haematopoiesis (for reviews see refs 1, 2). In vitro, leukaemia inhibitory factor, oncostatin M, ciliary neurotrophic factor and interleukin-11 display overlapping activities with IL-6. This functional redundancy may be explained by the interactions of specific binding receptors with a common signal-transducing receptor (gp130) (for reviews see refs 3, 4). To elucidate the unique function of IL-6 in vivo, we have disrupted the IL-6 gene by homologous recombination. IL-6-deficient mice develop normally. They fail to control efficiently vaccinia virus and infection with Listeria monocytogenes, a facultative intracellular bacterium. The T-cell-dependent antibody response against vesicular stomatitis virus is impaired. Further, the inflammatory acute-phase response after tissue damage or infection is severely compromised, whereas it is only moderately affected after challenge with lipopolysaccharide. We conclude that IL-6 production induced by injury or infection is an important in vivo SOS signal which coordinates activities of liver cells, macrophages and lymphocytes.
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PMID:Impaired immune and acute-phase responses in interleukin-6-deficient mice. 812 68


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