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 systemic BCG infection in mice induced multiple small granulomas located mainly in the periportal areas of the liver. Following systemic challenge of such mice with purified protein derivative of tuberculin (PPD), a rapidly developing hepatitis with diffuse intralobular mononuclear cell infiltration was precipitated, accompanied by high levels of aspartate transaminase in peripheral blood, hypoglycemia, focal hepatocyte necrosis, and accumulation of fibrinogen in liver. Bacterial lipopolysaccharide (LPS) also provoked acute hepatic damage both in BCG-infected mice and in mice pretreated with Corynebacterium parvum. PPD was not active in the latter. There were also lymphoid cell destruction and fibrinogen accumulation in the spleen of BCG-PPD-treated mice. Possible involvement of inflammatory and hepatotoxic mediators is suggested, and a T-lymphocyte-macrophage regulatory role in the pathogenesis of hepatitis is discussed.
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PMID:Tuberculin hypersensitivity hepatitis in mice infected with Mycobacterium bovis (BCG). 702 5

Bacterial lipopolysaccharide (LPS) stimulates pulmonary macrophages from BCG immune-rechallenged hamsters to kill tumor cells in vitro. However, pulmonary macrophages from BCG immune and from untreated hamsters cannot be activated for tumor cytotoxicity by in vitro treatment with LPS. Pulmonary macrophages from the nonimmune hamsters acquire tumoricidal capacity after 3 hr of coculture with T cells from BCG immune-rechallenged hamsters or when incubated with Con-A-stimulated spleen cell supernatant fluid. A heterogeneous population of pulmonary lavage cells from BCG immune and from BCG immune-rechallenged hamsters destroys the tumor cells more effectively than a homogeneous population of pulmonary macrophages from the same animals. LPS significantly augments the cytotoxic activity of the heterogeneous population of pulmonary lavage cells.
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PMID:The effects of lipopolysaccharide, BCG-immune T lymphocytes, and lymphokines on generations of tumoricidal pulmonary macrophages in Syrian hamster. 703 79

The effect of graded amounts of dietary lactalbumin (L) and casein (C) hydrolyzates on the immune responsiveness of C3H/HeN and DBA/2 strain mice has been investigated by measuring both the specific humoral immune response to sheep red blood cells (SRBC) and the nonspecific splenic cell responsiveness to phytohemagglutinin, concanavalin A and Escherichia coli lipopolysaccharide after stimulation with Mycobacterium bovis, strain BCG. The nutritional efficiency of these diets was similar at both 12 and 28% amino acid levels. The immune responses of mice fed the L diets were found to be significantly greater than those of mice fed the corresponding C diets, especially at the 28% level. Furthermore in the mice fed L diet, increasing the concentration of amino acid in the diet from 12 to 28% greatly enhanced immune responsiveness by both parameters measured. In the C-fed mice, a comparable enhancement of mitogen responsiveness with increasing amino acid level of diet was seen, but there was no change in the humoral immune response. The enhancement of immune responsiveness observed in mice fed the 28% L diet was moderately reduced by the addition of phenylalanine to the diet, indicating that the lower level of this amino acid in the L protein may be of some significance. These dietary effects on immune responsiveness were remarkably similar in both mouse strains tested.
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PMID:Influence of dietary proteins on the immune system of mice. 705 Mar 21

Peripheral macrophages (MO) from mice injected with proteose-peptone (P), thioglycollate (T) medium or BCG and from mice undergoing a graft versus host (GVH) reaction were tested for their cytotoxicity towards three murine tumour cell lines. The ability of lipopolysaccharide (LPS) and lymphokines to increase cytotoxicity was also studied. TMO were only slightly cytotoxic and this cytotoxicity was not enhanced by LPS and lymphokines. PMO showed the same degree of cytotoxicity as TMO, but this could be enhanced by LPS and lymphokines. Resident macrophages (RMO) sometimes resembled TMO and sometimes PMO. BCGMO were highly cytotoxic and could not be further activated by LPS and lymphokines. GVHMO were moderately cytotoxic but could not be further activated by LPS and lymphokines in contrast to the MO from hybrid controls.
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PMID:In vitro studies on the tumour cytotoxicity of normal, stimulated and immunologically activated mouse macrophages. 708 Aug 37

A variety of culture conditions were used to assess the lipopolysaccharide (LPS) response of spleen cells from several strains of Syrian hamsters. The cells failed to respond to LPS while good responses were obtained with Concanavalin A and poke week mitogen. Stimulation of macrophages with LPS failed to induce tumor cell destruction unless the macrophages were primed by immunization with BCG. The results indicated that hamsters are unresponsive to LPS.
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PMID:Lack of lipopolysaccharide response of inbred strains of Syrian hamsters. 709 33

A relatively large population of murine peritoneal exudate macrophages induced with viable BCG or heat-killed Corynebacterium parvum was stained by the antiserum prepared against purified gangliotetraosyl ceramide (asialo GM1), while only a small population of peritoneal resident macrophages or peritoneal exudate macrophages induced with proteose peptone was stained. The cytotoxicity assay of those macrophages with anti-asialo GM1 plus complement supported these results. Peritoneal macrophages induced with BCG or C. parvum showed strong cytotoxicity for EL4 cells in vitro, while resident or peptone-induced peritoneal macrophages showed no cytotoxicity. BCG- or C. parvum-induced peritoneal cells contained both NK cells and cytotoxic macrophages, and either in vivo or in vitro pretreatment of the cells with anti-asialo GM1 and complement abolished the activities of both types of cells. Peptone-induced peritoneal macrophages incubated with lymphokines (LK) or lipopolysaccharide (LPS) were cytotoxic for EL4 cells and contained an increased number of cells stained by anti-asialo GM1. The cytotoxicity of these in vitro activated macrophages was reduced by treatment with anti-asialo GM1 plus complement. When peptone-induced peritoneal macrophages were incubated with LK, the number of cells stained by anti-Ia antiserum increased, but the number did not increase when the macrophages were incubated with LPS. Pretreatment of peptone-induced macrophages with anti-asialo GM1 plus complement did not affect the ability of the macrophages to be activated by LK. These results taken together strongly suggest that the antigen(s) reactive with anti-asialo GM1 is expressed on the cell surface of cytotoxic peritoneal macrophages in mice.
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PMID:Appearance of a cell surface antigen associated with the activation of peritoneal macrophages in mice. 715 91

In an in vitro assay, malarial parasites (Plasmodium vinckei petteri) taken from mice 7 to 8 h after the injection of bacterial lipopolysaccharide (LPS) incorporated significantly less hypoxanthine into nucleic acid than did parasites from saline-treated controls. In contrast, incorporation was normal in parasites taken from mice within minutes of the injection of LPS and in parasites cultured with LPS. These results implied that the injection of LPS induced the release of mediators with a cytostatic effect on the parasite. This suggested an explanation for the protective action of LPS in malarial infections as well as for the "crisis forms" seen both in naturally resolving infections and in animals pretreated with such agents as BCG.
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PMID:Demonstration of a lipopolysaccharide-induced cytostatic effect on malarial parasites. 727 7

Serum from Mycobacterium bovis BCG-infected mice treated with lipopolysaccharide was cytotoxic to tumor cells in vitro. Serum-induced cytotoxicity was estimated by measuring release of [3H]thymidine into culture supernatants of prelabeled tumor target cells. Serum from BCG-infected mice not treated with lipopolysaccharide or from uninfected mice treated with lipopolysaccharide was inactive. Moreover, although serum cytotoxic activity was evident with 10 syngeneic or allogeneic tumor cell lines, little or no effect was observed with normal embryonic fibroblast target cells. Maximal titers of serum cytotoxic activity were detected 14 days after BCG infection and 2 h after LPS treatment. Serum of BCT-infected, T-cell-deficient nude mice developed strong cytotoxic activity after LPS treatment; however, lipopolysaccharide-insensitive C3H/HeJ mice could produce this cytotoxic activity only after adoptive transfer with lipopolysaccharide-responsive C3H/HeN bone marrow. Physicochemical characterization of the serum cytotoxic activity revealed a heat-stable (56 degrees C, 30 min) entity with a molecular weight of about 60,000 and an isoelectric point at pH 4.8. Biological and physicochemical characteristics of this serum cytotoxic activity as defined by an in vitro assay were very similar to characteristics of tumor necrosis factor and suggest that this molecule may be a major effector mechanism for the antitumor actions of lipopolysaccharide.
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PMID:Generation and characterization of a lipopolysaccharide-induced and serum-derived cytotoxic factor for tumor cells. 738 May 63

Production of nitric oxide (NO) by macrophages is important for the killing of intracellular infectious agents. Interferon (IFN)-gamma and lipopolysaccharide stimulate NO production by transcriptionally up-regulating the inducible NO synthase (iNOS). Macrophages from mice with a targeted disruption of the IFN regulatory factor-1 (IRF-1) gene (IRF-1-/- mice) produced little or no NO and synthesized barely detectable iNOS messenger RNA in response to stimulation. Two adjacent IRF-1 response elements were identified in the iNOS promoter. Infection with Mycobacterium bovis (BCG) was more severe in IRF-1-/- mice than in wild-type mice. Thus, IRF-1 is essential for iNOS activation in murine macrophages.
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PMID:Requirement for transcription factor IRF-1 in NO synthase induction in macrophages. 751 Apr 19

Guinea pigs were given a preparatory injection of heat-killed Mycobacterium tuberculosis in a water-in-mineral oil emulsion into the footpads. A provocative injection of muramyldipeptide given 3-8 weeks later into the flanks, caused severe inflammation, with hemorrhage and necrosis and necrosis at the footpads. In this study, we determined the features of the preparatory injection required to prepare the necrotic reaction. Most mycobacteria-related and Gram-negative bacteria were capable of preparing guinea pigs for the necrotic reaction upon provocative injection with muramyldipeptide, whereas Gram-positive bacteria did not. Boivin- and Morrison-type lipopolysaccharides, which have a high content of bacterial protein, induced the susceptibility, whereas Westphal-type lipopolysaccharide, which has a low level of the protein, did not. Moreover, the latter adjuvant-active lipopolysaccharide and muramyldipeptide together with ovalbumin also exerted the activity. The development of delayed-type hypersensitivity to the protein antigen seemed to be important for inducing the necrotic reaction. Mice, rats, rabbits and monkeys were injected in the same way as the guinea pigs. The necrotic reaction occurred in the flanks of the monkeys, but not in the other animals. A similar necrotic reaction also occurred in the flanks of guinea pigs given live BCG cells in phosphate-buffered saline as well as the heat-killed M. tuberculosis in water-in-mineral oil emulsion upon provocative injection with muramyldipeptide. These findings suggested that the induction is associated with the development of delayed-type hypersensitivity to the protein antigen administered in the preparatory injection [corrected].
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PMID:Guinea pigs prepared with various bacteria and their components to induce a necrotic reaction provoked with muramyldipeptide. 786 50


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