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)

(DBA/N[female] X CBA/2[male])F1 males have been reported to be deficient in producing antibodies against a number of antigens, including carbohydrates (I. Scher, Adv. Immunol. 35:1-71, 1982). We show that F1 male mice, in contrast to females, made less lipopolysaccharide (LPS)-specific antibodies after immunization with heat-inactivated Pseudomonas aeruginosa and had significantly less naturally occurring LPS-specific antibodies. Furthermore, neutropenic males were 50 to 1,000 times more sensitive to challenge with representative isolates belonging to the seven Fisher immunotypes. Administration to neutropenic F1 males of a human monoclonal antibody specific for the O carbohydrates of P. aeruginosa immunotype 2 LPS or administration of serum from rabbits immunized with heat-inactivated P. aeruginosa immunotype 1 raised the level of resistance to bacterial challenge close to that of females. The results show that the X-linked immunodeficient mouse is an excellent model with which to test the protective efficacy of P. aeruginosa-specific monoclonal antibodies.
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PMID:X-linked immunodeficient mice as a model for testing the protective efficacy of monoclonal antibodies against Pseudomonas aeruginosa. 312 80

Macrophage activation by a traditional Chinese herbal medicine, xiao-chai-hu-tang (Japanese name: shosaiko-to), was investigated. Intraperitoneal (i.p.) administration of shosaiko-to into (BALB/c x DBA/2)F1 mice resulted in marked activation of macrophages with respect to phagocytic and lysosomal enzyme activities (acid phosphatase and N-acetyl-beta-D-glucosaminidase) compared with the control. The maximal responses were induced by an i.p. injection of 3 mg shosaiko-to 4 days previously. Enhanced activities induced by shosaiko-to were also seen in C3H/HeJ mice, which is a non-responder strain to bacterial lipopolysaccharide (LPS). Significant macrophage accumulation in the peritoneal cavity and increased lysosomal enzyme activities were observed in mice injected with shosaiko-to. Shosaiko-to exhibited significant cytostasis-inducing activity. In addition, the administration of shosaiko-to led to a moderate expression of Ia antigen on the surface of peritoneal macrophages. These results suggest that shosaiko-to is a potent macrophage activator.
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PMID:Activation of murine peritoneal macrophages by intraperitoneal administration of a traditional Chinese herbal medicine, xiao-chai-hu-tang (Japanese name: shosaiko-to). 317 54

Anti-mu preparations differ greatly in their ability to stimulate mouse B cells to incorporate tritiated thymidine (TdR). We have found that these differences may be due in part to different levels of lipopolysaccharide (LPS) content. In this report we show that LPS concentrations as low as 0.025 ng/ml stimulate the proliferation of T-depleted (C57BL/6 X DBA/2)F1 (B6D2F1) spleen cells, provided that 5 X 10(-5) M 2-mercaptoethanol is also present. Each of six commercial anti-mu preparations tested for LPS content contained more than this amount. We describe a technique that uses polymyxin B-agarose to remove nanogram quantities of LPS from anti-mu preparations. In B6D2F1 B cells, LPS-depleted anti-mu preparations induced much more uniform tritiated thymidine incorporation than did non-depleted preparations; but there was little difference between the two preparations when tested on B cells from C3H/HeJ (LPS hyporesponsive) mice.
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PMID:The influence of lipopolysaccharide content on the apparent B cell stimulating activity of anti-mu preparations. 325 11

We have produced monoclonal antibodies (MoAb) to the Rb core and lipid A regions of Salmonella lipopolysaccharide (LPS) and have assessed their ability to inhibit LPS-mediated mitogenic responses in vitro, and to protect against LPS toxicity and lethal Salmonella infection in vivo. Monoclonal antibodies RC-8 and RC-16 were specific for LPS Rb core determinants, and MoAb LA-1, LA-2, LA-3, LA-4 and LA-5 were specific for lipid A. Anti-lipid A MoAb LA-2, LA-3 and LA-5 were found to abrogate mitogenic responses of C3H/HeN spleen cells to smooth S. typhimurium LPS (S LPS) and to rough S. minnesota R595 LPS (Re LPS). Monoclonal antibody LA-5 was effective in extending the median length of survival of C3H/HeN mice challenged with a lethal dose of either S LPS or Re LPS. Antibody LA-2 could extend the median length of survival of C3H/HeJ mice challenged with Re LPS but not with S LPS, and failed to extend significantly the length of survival of S LPS-challenged C3H/HeN and DBA/2 mice. Neither 20 micrograms of anti-Rb core or anti-lipid A MoAb nor 200 micrograms of anti-lipid A MoAb were able to protect C3H/HeN or BALB/c mice, respectively, against lethal infection with S. typhimurium SR-11. These results suggest that the importance of anti-lipid A antibodies in host defence may lie more in their ability to neutralize pathological effects of LPS, than in their ability to protect against bacterial infection.
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PMID:Monoclonal antibodies to salmonella lipopolysaccharide: functional analysis of anti-lipid A antibodies. 329 50

Lipid X (2,3-diacylglucosamine 1-phosphate) is a novel monosaccharide precursor of lipid A (the active moiety of gram-negative endotoxin) and has been found to be protective against endotoxin administered to mice and sheep and against life-threatening gram-negative infections in mice. Because of the need to design optimal dosing regimens in experimental models of ovine and murine septicemia, the pharmacokinetic profile of lipid X was investigated in sheep and in two strains of mice by using 32P-labeled lipid X. In sheep, peak whole blood lipid X levels after a bolus injection of 100 micrograms of lipid X per kg were 900 ng/ml. An initial rapid distribution phase of 7.98 +/- 0.1 min was observed, followed by a prolonged elimination phase of 3.0 +/- 0.5 h; the area under the curve from time zero to infinity was 428 +/- 27 ng.h/ml. The serum half-lives of lipid X were slightly shorter than whole blood half-lives, suggesting that lipid X associates with cellular elements. Metabolites of lipid X could not be detected in serum over a 4-h period. Lipid X appears to accumulate mainly in the liver, and the tissue distribution of lipid X resembles that of lipopolysaccharide. The elimination rate of lipid X in mice was approximately four times as rapid as that seen in sheep. Lipid X pharmacokinetics in lipopolysaccharide-sensitive DBA/2J mice were virtually identical with those seen in endotoxin-resistant C3H/HeJ mice. The pharmacokinetics described here should greatly aid in the design and interpretation of animal studies investigating the therapeutic applications of lipid X in gram-negative septicemia.
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PMID:Elimination and tissue distribution of the monosaccharide lipid A precursor, lipid X, in mice and sheep. 334 11

Experimental liver injury was produced in mice by the immunological technique. The utility of these models as an immunopharmacological method was investigated. The first model was produced by the injection of anti-basic liver protein (BLP) rabbit antibody into DBA/2 mice that had been previously immunized with rabbit IgG. The second liver injury was caused by injection of anti-liver specific protein (LSP) rabbit antibody into DBA/2 mice. The third model was produced by the injection of bacterial lipopolysaccharide (LPS) into Corynebacterium parvum pretreated ddY mice. In all injury models, extensive liver parenchymal cell damage was estimated by elevation of glutamate transaminase (GOT and GPT) activity. These were confirmed by histopathological studies of the liver. Typical histopathological changes in the liver from injured mice were submassive hepatocellular necrosis and infiltration of granulocytes and lymphocytes into the portal tract and sinusoid in the necrotic lesion. Administration of prednisolone and cyclophosphamide for 10 days prior to injection of eliciting antibodies or LPS suppressed the elevation of serum transaminase levels in all experimental liver injury models. Cianidanol and sylibin inhibited the elevation of GOT and GPT in anti-BLP induced liver injured mice. These evidences suggest that the above models are suitable for investigating the remedy for liver diseases.
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PMID:Liver injury model in mice for immunopharmacological study. 337 35

We have analyzed gastrointestinal immune function in both DBA/2 and spontaneously autoimmune New Zealand Black (NZB) mice. We have studied both in vitro proliferation and differentiation of Peyer's patch cells and have measured immunoglobulin (Ig) secretion by cultured jejunal segments. Peyer's patch B cells and T cells from both DBA/2 and NZB mice showed similar proliferative responses to Con A and lipopolysaccharide (LPS), respectively. Unlike NZB splenic B cells, isolated Peyer's patch B cells from NZB mice did not spontaneously secrete Ig of any isotype. Seven-day cultures of equal numbers of Peyer's patch T cells and B cells resulted in similar patterns of secretion of IgA, IgG, and IgM in both strains. The addition of Con A to cultures of DBA/2 Peyer's patch cells consistently resulted in a onefold to threefold increase in IgA secretion after 7 days. Con A stimulation of NZB Peyer's patch cells did not produce any increment in IgA secretion. LPS stimulation of Peyer's patch cells from either strain resulted in a similar increase in IgG secretion with little effect on IgA secretion. The in vivo correlate of this finding was seen in the IgA to IgG ratio of Ig secreted by cultured jejunal fragments. In DBA/2 mice the rates of IgA/IgG varied from 2.36 to 4.85, whereas in NZB mice the ratio never exceeded 0.5. These experiments show that defects on the T cell compartment of NZB mice encompass gut-associated lymphoid tissue. The possible relationship of these findings and previously observed defects in oral tolerance is discussed.
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PMID:Analysis of T cell and B cell function in Peyer's patch and lamina propria of New Zealand Black and DBA/2 mice. 348 25

Strain differences were investigated on the proliferative responses of splenic lymphocytes obtained from C3H/He, BALB/c, and DBA/2 mice that were treated with cadmium (Cd) for 5 days (0.5 or 1.0 mg Cd/kg/day, sc), and the results were compared with those of in vitro treatment of spleen cells with Cd. Following in vivo treatment, splenocytes from the C3H strain were significantly more susceptible to suppressive effects of Cd exposure on all indices for proliferative responses to mitogens (concanavalin A, phytohemagglutinin, and lipopolysaccharide) and allogeneic lymphocytes, while those from DBA and BALB strains were fairly resistant. Among the three strains, the highest Cd concentrations in plasma and spleen were obtained in the C3H strain with the lowest hepatic concentration of Cd. On the other hand, the Cd exposure hardly affected the splenic concentration of zinc in the C3H strain in contrast to its decrease in the others. When spleen cells obtained from normal mice were treated in vitro with Cd, the C3H strain was more resistant to the suppressive effect of Cd than the other strains. These results indicate that the mouse strain variations in Cd-mediated suppression of lymphocyte proliferation are not based on intrinsic lymphocyte sensitivities, but likely are due to differences in the metabolism of Cd, which is under genetic control.
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PMID:Strain differences in cadmium-mediated suppression of lymphocyte proliferation in mice. 348 42

Suramin stimulated DNA synthesis in spleen cell cultures of all inbred strains of mice tested, including, for example, CBA, DBA/2, C57BL/6, and the lipopolysaccharide (LPS)-nonresponsive strain C3H/HeJ. The cells responding to the drugs were removed by passage through nylon wool columns, but they were not eliminated by in vivo treatment of the mice with anti-Thy 1.2 antibody. Spleen cells of homozygous nude mice (C57BL/6 or BALB/c background) were as reactive as those of their heterozygous littermates. Collectively the data show that suramin is a B-cell mitogen in the mouse.
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PMID:Activation of murine B lymphocytes by suramin. 348 56

Accumulation of lymphocytes after an intraperitoneal (ip) injection of a traditional Chinese herb medicine, XIAO-CHAI-HU-TANG (Japanese name: shosaiko-to), was investigated. Shosaiko-to induced marked accumulation of lymphocytes rather than macrophages in the peritoneal cavity of ICR mice, whereas various kinds of irritants, e.g. proteose-pepton, Escherichia coli lipopolysaccharide (LPS), OK-432 and Corynebacterium parvum, induced preferential accumulation of macrophages rather than lymphocytes. By means of analysis using two-color fluorescence-activated cell sorter (FACS), it was revealed that the increased lymphocyte subpopulations not only in the peritoneal cavity but also in the spleen of C3H/He mice by the injection of shosaiko-to were comprised of both immature B (IgM+ and IgD-) and null (thyl- and Ig-) cells. This effect of shosaiko-to was observed in other C5 normal strains, C3H/HeJ (LPS-nonresponder), C57BL/6, BALB/c and athymic nu/nu (ICR background) mice, but not in C5 deficient strains, AKR/J, A/J and DBA/2 mice, indicating that the accumulation of immature B and null cells in the periphery induced by shosaiko-to is closely related to the complement system.
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PMID:Accumulation of immature B and null lymphocytes in the periphery after intraperitoneal administration of traditional Chinese medicine, xiao-chai-hu-tang (Japanese name: shosaiko-to). 349 65


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