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)

Previous studies in our laboratory have indicated that naturally resistant, inbred DBA/2J mice mount a greater serum antibody response to Pseudomonas aeruginosa 19660 than susceptible C57BL/6J mice. However, the specificity of the antibody produced was not known. The present study examines the specificity and kinetics of the humoral response of these mouse strains to potential virulence factors produced by the organism during both a primary and a secondary corneal infection administered 4 weeks after the primary infection. Serum antibody levels specific for lipopolysaccharide (LPS), exotoxin A, phospholipase C (PLC), alkaline protease, elastase, and flagella were measured by enzyme-linked immunosorbent assay. Little or no antibody to either alkaline protease or elastase was detected during either primary or secondary infection. Immunoglobulin G (IgG) antibodies specific to exotoxin A, PLC, and flagella were detected 2 weeks after primary infection, and a rapid response to these antigens was measured 1 week after secondary infection. During primary infection, detectable LPS-specific antibody was only IgM, while IgG appeared only after secondary infection. The kinetics of the humoral response in susceptible C57BL/6J mice were similar to those in resistant DBA/2J mice, although the magnitude of the response varied according to the antigen tested. These results indicate that LPS, exotoxin A, PLC, and flagella are present or produced in amounts that are immunogenic during corneal infection by P. aeruginosa 19660 in the mouse strains tested.
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PMID:Serum antibody response to Pseudomonas aeruginosa antigens during corneal infection. 190 70

The effect of mercuric chloride on mitogen-induced DNA synthesis was investigated using lymphocytes from SJL and DBA mice, which are known to be susceptible and resistant to induction of autoimmunity by mercury, respectively. Treatment of SJL mice with 5 ppm mercuric chloride in their drinking-water for 2 wk resulted in a two- to three-fold increase of concanavalin A and lipopolysaccharide-induced thymidine incorporation in splenocytes. Mitogen-induced thymidine incorporation in splenocytes from identically treated DBA mice was not significantly different from that seen in controls. In vitro treatment of splenocytes from SJL mice with mercury caused a dose-dependent increase of concanavalin A-, lipopolysaccharide and phytohaemagglutinin-induced thymidine incorporation. This effect was optimal when 10(-7)-10(-8) M-mercuric chloride were added as a pulse 1 hr before the addition of mitogens, whereas higher and lower concentrations were less effective. The mitogen-induced DNA synthesis in splenocytes from DBA mice was either not affected by the addition of mercuric chloride or decreased by higher mercury concentrations. The addition of mercury to thymocytes from DBA and SJL mice caused a slight and moderate increase, respectively, in concanavalin A-induced thymidine incorporation.
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PMID:Strain differences in the effect of mercury on murine cell-mediated immune reactions. 193 95

When Dengue type 2 virus (DEN-2) is put in contact with spleen cells from DBA/2 mice that had been stimulated with Concanavalin A, it was found a decrease in the incorporation of (3H) Thymidine. Furthermore it was observed that the number of Antibody forming cells (Plaque forming cells) against SRBC was decreased, when lymphocytes from DBA/2 mice spleen in culture, had been stimulated with sheep red blood cells (SRBC) in vitro and then infected with DEN-2 virus and the interleukin-1 (IL-1) biosynthesis was quantified in the thymocyte system it was shown that macrophages produced high levels of IL-1 compared with non-infected cells, and that this increased levels could be similar to that produced when macrophages are stimulated with lipopolysaccharide form E. Coli (LPS). The above mentioned results suggest that DEN-2 virus is able of altering some functions of the immune response concerning T and B lymphocytes. Furthermore, the infection of P388D1 cells induce in the first 24 hours an over production of IL-1 that could be the reason why in the natural infection in humans, patients run a fever in the beginning of the viremia caused by DEN-2 virus related with the property of IL-1 reported as endogenous pyrogen.
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PMID:[Effect of in vitro infection with dengue virus (DEN-2) on various cellular immune response functions in the mouse]. 210 11

The possible involvement of tumor necrosis factor-alpha (TNF) in the metabolic disturbances induced by anti-CD3 monoclonal antibodies (mAb) was analyzed in DBA/2 mice injected with 50 micrograms of the anti-murine CD3 mAb 145-2C11. First, we found that 145-2C11 induces a profound hypothermia maximal between 3 h and 6 h after the injection (at 3 h: -3.0 +/- 0.1 degrees C) as well as hypoglycemia (blood glucose levels at 6 h and 24 h: 76 +/- 13 mg/100 ml and 92 +/- 22 mg/100 ml, respectively, p less than 0.001 as compared with control values). These metabolic changes are preceded by the release of TNF into the circulation (peak serum TNF levels at 2 h: 50 +/- 23 pg/ml, p less than 0.01 as compared with controls). The release of TNF induced by 145-2C11 depends on the effect of the mAb on T cells as it is not observed in athymic nude mice while lipopolysaccharide-resistant C3H/HeJ mice also display a significant rise in serum TNF (peak levels at 2 h: 59 +/- 44 pg/ml). Pretreatment of DBA/2 mice with 12 mg of rabbit anti-murine TNF antibodies completely prevents the hypothermia while the hypoglycemia is significantly attenuated. Finally, F(ab')2 fragments of 145-2C11 induce only a transient hypoglycemia (blood glucose levels at 6 h: 109 +/- 14, p less than 0.001 as compared with controls) but neither hypothermia nor significant TNF release. We conclude that TNF is a major mediator of the acute metabolic changes induced by the intact form of 145-2C11.
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PMID:Hypothermia and hypoglycemia induced by anti-CD3 monoclonal antibody in mice: role of tumor necrosis factor. 213 64

Social conflict stress was examined for its effects on in vitro and in vivo immunity in mice. Adaptive immunity, as measured by the generation of primary IgM antibody responses to the T-dependent antigen keyhold limpet hemocyanin, was suppressed following chronic (greater than 1 day), but not acute (less than 1 day), stress periods while the IgM response to the T-independent antigen polyvinylpyrrolidone was not affected. In vitro proliferative responses of splenocytes to the T cell mitogen concanavalin A and the B cell mitogen lipopolysaccharide were unaffected. Acute (less than 1 day) stress dramatically increased innate immunity as measured by a luminol-dependent chemiluminescence assay of phagocytic cell function. DBA/2J mice averaged a 269% increase in phagocytosis as compared to a 412% increase in C57BL/6J. This differential effect of stress on immune responsiveness indicates that alterations in innate immunity in addition to adaptive immunity should also be considered when evaluating neuroendocrine and immune interactions in response to stress.
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PMID:Innate and adaptive immune responses in a social conflict paradigm. 239 33

Periodontal disease is a chlonic inflammatory disorder, and for which oral microbes are supposed to be responsible. Among oral microbials, gram-negative bacterias have been studied extensively in relation to periodontal disease for their pathogenicity due to their lipopolysaccharide (LPS), exocellular enzymes or bacterial toxin. As for gram-positive bacterials, it has been reported recently that gram-positive bacteria can elicit immunological responses, and this may be responsible for the initiation and/or development of periodontal disease. However, precise mechanisms of bacterial action, especially of gram-positive bacteria, on periodontal disease have not been elucidated yet. In this experiment, therefore, gram-positive bacteria (S. epidermidis), peptidoglycan subunits of S. epidermidis (SEPS) and muramyl dipeptide (MDP) were used to investigate for their activities to stimulate spleen mononuclear cells to replicate and produce various kinds of cytokines. Immunological responsibilities of various strains of mice were explored to investigate the difference of defence of mechanisms. Following results were obtained. (1) S. epidermidis itself showed a extremely low cell-mediated activity to stimulate the replication of spleen mononuclear cells in contrast to E. coli. Staphylococcal phage lysate and SEPS stimulated remarkally the replication of spleen mononuclear cells. (2) The stimulation of spleen mononuclear cells was accompanied by the production of interleukin 3 (IL-3) and colony stimulating factor (CSF), but interleukin 2(IL-2) was not produced as in the case of E. coli. (3) Analysis of cell surface antigens revealed the increase of the numbers of Ia+ and Mac-2+ bone marrow cells following stimulation of spleen mononuclear cells with SEPS. However, T or B cells were not increased. (4) Macrophage-depleted and antisera Ia-treated spleen mononuclear cells showed a marked decrease of replicating activity of spleen mononuclear cells. (5) Among the various strains of mice tested C3H/HeN, Balb/c, AKR, DBA/2, C57BL/6, ddY, C3H/HeJ, MRL/lpr and showed a high immunological responses, but Balb/c did not. C3C/HeJ and MRL/lpr also lacked immunological reactivity. These results suggest that proliferative response of lymphocyte with peptidoglycan in gram-positive bacterium is very important for infection and its defensive reaction against gram-positive bacteria.
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PMID:[Mechanism of stimulation of spleen mononuclear cells by gram-positive bacterial peptidoglycan]. 248 94

Histoplasma capsulatum, a facultative intracellular parasite of macrophages, grows within mononuclear cells of the P388D1 and IC-21 cell lines with a generation time comparable to that with which it grows in normal resident peritoneal macrophages (10 +/- 2 h). Recombinant murine gamma interferon (rMuIFN-gamma) activates P388D1 cells to express la antigens but not to inhibit the intracellular growth of H. capsulatum, alone or in combination with lipopolysaccharide. IC-21 cells also could not be activated to fungistasis with rMuIFN-gamma. Explanted resident peritoneal macrophages of the C57BL/6 (from which the IC-21 cell line derives), C3H/HeJ, DBA/2 (from which the P388D1 cell line derives), A/J, and SJL/J strains of mice were all stimulated by rMuIFN-gamma to inhibit the fungus.
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PMID:Macrophage cell lines P388D1 and IC-21 stimulated with gamma interferon fail to inhibit the intracellular growth of Histoplasma capsulatum. 250 48

The effects of OKY-046, a selective thromboxane A2 (TXA2) synthetase inhibitor, and ONO-3708, a novel TXA2 receptor antagonist, on liver disease were investigated in mice. The liver injury was induced by either an injection of antibasic liver protein (BLP) antibody into DBA/2 mice that had been previously immunized with rabbit IgG or by an injection of bacterial lipopolysaccharide (LPS) into Corynebacterium parvum (C. parvum) pretreated DDY mice. 1) In both injury models, clear elevation of glutamate transaminase (GOT and GPT) activity due to extensive liver parenchymal cell damage was observed; this was confirmed by significant histopathological changes in the liver. 2) Typical histopathological changes in the liver were submassive hepatocellular necrosis in the anti-BLP antibody-induced injury model and focal necrosis in the LPS-induced model. Inflammation and increased cell infiltration in portal connective tissue were observed in both cases. 3) Administration of OKY-046 (50 mg/kg) and ONO-3708 (0.5, 1.0 and 2.0 mg/kg) suppressed the elevation of serum GOT and GPT levels and histopathological changes in both experimental liver injury models. 4) Indomethacin inhibited the development of liver disease caused by anti-BLP antibody but not by bacterial LPS. Prostaglandin I2 inhibited the elevation of serum GOT and GPT levels and histopathological changes of the liver in the mice treated with anti-BLP antibody and showed the tendency to inhibit the development of liver injury caused by bacterial LPS.
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PMID:Effect of OKY-046 and ONO-3708 on liver injury in mice. 251 4

The intratumoral administration of lipopolysaccharide (LPS) and muramyl dipeptide (MDP) in combination, but not separately, resulted in necrosis and rejection of subcutaneous P815 mastocytoma nodules in DBA/2 mice with 30 to 40% survival. Previous sensibilization of animals by LPS + MDP, treatment by indomethacin, cyclophosphamide or syngeneic lymphocytes did not augment the immunotherapeutic action of LPS + MDP combination. Reinoculation of P815 cells into cured DBA/2 mice 8 months after the disappearance of the primary tumor led to rejection of new nodules with 50% survival rate. In LPS + MDP immunotherapy of these tumors two stages may be distinguished by a thrombo-necrotic stage and that of development of immunity.
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PMID:[The synergistic action of lipopolysaccharide and muramyl dipeptide in the immunotherapy of DBA/2 mice with mastocytoma P815]. 251 87

The objective of this study was to determine the effect of delta-9-tetrahydrocannabinol (delta-9-THC), the major psychoactive component of marihuana, on macrophage protein expression in response to bacterial immunomodulators. Peritoneal macrophages of (B6C3)F1 mice receiving Propionibacterium acnes exhibited a novel protein profile when compared to resident or vehicle-treated macrophages. In contrast, macrophages from mice treated with P. acnes in concert with delta-9-THC exhibited profiles for which the majority of protein species reverted to patterns seen in profiles of resident or vehicle-treated macrophages. Treatment of the murine macrophage line P388D1 (DBA/2) in vitro with bacterial lipopolysaccharide (LPS) resulted in the hyperproduction of a subset of proteins ranging from 73 to 18 kD relative molecular weight. Coexposure of the P388D1 cells to LPS and 10(-7) M to 10(-5) M delta-9-THC resulted in a dose-related depletion of these proteins. These results suggest that delta-9-THC suppresses the expression of proteins elicited by macrophage bacterial immunomodulators.
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PMID:Delta-9-tetrahydrocannabinol inhibits macrophage protein expression in response to bacterial immunomodulators. 253 3


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