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 lipophilic thermostable lipopolysaccharide (LPS) complex was isolated by phenol extraction from purified suspensions of the typhus group rickettsiae. The LPS complex is antigenic and possesses some endotoxic properties such as toxicity for actinomycin D-treated mice, pyrogenicity for rabbits and guinea pigs, ability to elicit hypothermia in white rats and local Schwartzman reaction and active cutaneous anaphylaxis in rabbits.
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PMID:Some biological properties of an endotoxic lipopolysaccharide from the typhus group rickettsiae. 2 40

An antigen (ZAB) common to Neisseria gonorrhoeae was prepared by stepwise elution of a crude gonococcal antigen (ZA) from columns of diethylaminoethyl cellulose employing 0.02 M phosphate buffers, pH 7.6, containing increasing concentrations of sodium chloride. Rats immunized with ZAB produced reaginic (IgE) antibody which cross-reacted with ZA prepared from eight gonococcal strains by the passive cutaneous anaphylaxis (PCA) test. Heating of the sera at 56 degrees C for 4 h destroyed the PCA activity. The PCA activity of the anti-ZAB rat serum was removed after absorption with ZAB antigen or with rabbit anti-rat IgE but not after absorption with gonococcal lipopolysaccharide or with heat-killed or formalinized gonococci. Treatment of ZAB with trypsin or heating at 100 degrees C for 30 min destroyed or reduced the antigenic activity respectively. Further purification of ZAB by filtration through Sephadex G-100 gave a preparation (ZAB2) which contained the common antigen as shown by the cross-reactivity of anti-ZAB2 rat serum with seven stains of N. gonorrhoeae. Fraction ZAB2 contained material which had a molecular weight less than 13,700 and was associated with the presence of material absorbing at 260 nm. The results of this study indicate that a low molecular weight antigen, which appears to be protein in nature and associated with nuclei acid, is common to the gonococcus and is the main antigenic component inducing reaginic (IgE) antibody in the rat.
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PMID:Induction of reaginic (IgE) gonococcal antibodies in the rat by a common antigen of Neisseria gonorrhoeae. 10 9

Cutaneous hypersensitivity responses to brucella antigens of different composition were studied in guinea pigs sensitized by infection with smooth brucella or immunization with killed rough brucella in adjuvant. These animals had circulating antibodies to smooth lipopolysaccharide or protein antigens, respectively. Intradermal skin tests, active cutaneous anaphylaxis, passive cutaneous anaphylaxis, and immunodiffusion tests were performed. Delayed-type hypersensitivity reactions uncomplicated by accompanying antibody-mediated reactions were seen only in infected guinea pigs with protein antigen that was entirely free of lipopolysaccharide. In the adjuvant-immunized animals, the protein antigen evoked overlapping antibody-mediated and delayed-type reactions. Lipopolysaccharide and polysaccharide preparations contained varying amounts of protein components. In infected animals, reactions of these antigens were clearly antibody mediated, but participation of delayed-type hypersensitivity could not be excluded. In adjuvant-immunized animals, the antibody-mediated reaction to the lipopolysaccharide preparation was caused by its protein component.
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PMID:Antibody-mediated and delayed-type hypersensitivity reactions to Brucella skin test antigens in guinea pigs. 80 71

Heat-labile, rat skin-fixing antibodies were detected readily in the sera of young female mice dosed intranasally with the body fluid of Ascaris suum (ABF) and the adjuvant, Bordetella pertussis vaccine (BPV). In addition, washed cell suspensions prepared from spleen and the lymph nodes regional to the lungs were positive in an adoptive cutaneous anaphylaxis assay, an assay which may detect activities of reagins associated with mast cells rather than reaginic antibody-secreting cells. The intraperitoneal route was a poor means of inducing circulating anti-ABF reagins and an intraperitoneal injection of ABF + BPV delayed the appearance of circulating reagins in mice dosed at the same time with ABF + BPV intranasally. Hypothymic female BALB/c. nu/nu ('nude') mice failed to produce circulating reagins to ABF but an injection of normal thymocytes or cortisone-resistant thymocytes from syngeneic female mice led to higher titers of circulating reagins than found in normal female BALB/c. nu/+ littermates. Using cells from young male or female syngeneic donors and male and female BALB/c. nu/mu recpiients, evidence was obtained for a defect in the thymus of young male mice and conceivably this defect may extend to the peripheral T cell population in such mice. Cyclophosphamide pretreatment or adrenalectomy increased circulating reagin titers in normal mice dosed intranasally with ABF + BPV, and pretreatment with lipopolysaccharide intranasally markedly reduced titers of circulating anti-ABF reagins. In the discussion, emphasis is given to the hypothesis that potent allergens are T cell-stimulating, relatively persistent antigens which, when located in submucosal lymphoid sites and under conditions of limited antibody production as a result of limited recruitment of 'helper' T cells systemically, lead to the induction and sustained production of IgE by resident Bxi cells and their progeny.
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PMID:Studies on immune responses to parasite antigens in mice. II. Aspects of the T cell dependence of circulating reagin production to Ascaris suum antigens. 108 24

The vasodilator bradykinin (Bk) has long been though to participate in shock induced by endotoxemia, anaphylaxis and acute pancreatitis. Recently developed kinin antagonists have made it possible to test this hypothesis. We studied the effect of two of them. DArg0Hyp3-Thi5.8-DPhe7-Bk (45 and 220 micrograms/kg/min) and Lys-Lys-Hyp2-Thi5.8-DPhe7-Bk (100 micrograms/kg/min) on the early hypotensive response to Escherichia coli lipopolysaccharide (LPS). Rats infused with the antagonist vehicle were used as controls. At 45 micrograms/kg/min, DArg0-Hyp3-Thi5.8-dPhe7-Bk prevented the hypotensive response to high doses of Bk; however, neither antagonist prevented the hypotensive response to LPS. Circulating kinins measured 3 min after injecting LPS or vehicle were similar (16.3 +/- 1.4 vs. 26.0 +/- 7.2 pg/ml; P greater than .23). In allergically sensitized rats, 500 micrograms/kg/min DArg0-Hyp3-Thi5.8-DPhe-7-Bk did not alter the hypotensive (anaphylactic) response to antigen challenge (P greater than .38). Similarly, hypotension caused by development of acute pancreatitis in rats was not prevented by infusion of DArg0-Hyp3-Thi5.8-DPhe7-Bk at 200 micrograms/kg/min, 10 min) (P greater than .69). These results indicate that in the rate formation of kinins is not a major contributor to the hypotensive response observed in early endotoxemia, anaphylaxis and acute pancreatitis.
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PMID:Kinin antagonist does not protect against the hypotensive response to endotoxin, anaphylaxis or acute pancreatitis. 281 Jan 21

The effect of several anti-atherogenic drugs (ticlopidine, nicotinic acid and etofibrate) on immune responses and immune complex anaphylaxis has been studied in mice. All the drugs enhanced the activation by concanavalin A, phytohemagglutinin, and lipopolysaccharide of lymphocytes taken from treated animals. Contact hypersensitivity to trinitrochlorobenzene was inhibited by similar treatments with the same drugs, possibly through inhibition of the efferent phase of the reaction. Nicotinic acid produced a slight enhancement of antibody responses to sheep erythrocytes, whereas etofibrate inhibited the response at the highest dose studied. In addition, treatment with these drugs variably protected the mice from anaphylactic shocks induced by immune complexes. Marked protection was also observed using the antiserotoninic, cyproheptadine. These results indicate that drugs used to prevent atherogenic processes modulate different proliferative and effector immunological reactions.
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PMID:Immunomodulatory activity of anti-atherogenic drugs: effects on blastogenesis, humoral response, delayed hypersensitivity and passive anaphylaxis by immune complexes. 298 56

Immune responses of mast cell-deficient WBB6F1-W/Wv mice and their mast cell-sufficient littermates (LM: WBB6F1-W/+, Wv/+ and +/+) were compared. After a single intravenous injection of sheep erythrocytes (SE), polyvinylpyrrolidone or bacterial lipopolysaccharide, the antigen-specific IgM plaque-forming cell (PFC) response of W/Wv mice was similar to or greater than the response of LM mice. When both primary and secondary injections of SE or chicken gamma-globulin were given to mice and antigen-specific IgG PFC responses quantified, the response of W/Wv again was similar to or greater than that of LM mice. Serum titers of antigen-specific IgE were higher in W/Wv than in LM mice after injections of ovalbumin in alum or infections of Nippostrongylus brasiliensis. Ovalbumin-sensitized W/Wv and LM mice developed active systemic anaphylaxis after ovalbumin challenge. The ability of W/Wv mice to be sensitized for and elicit contact sensitivity (CS) reactions was studied using picryl chloride or dinitrofluorobenzene as sensitizing and challenge agents and quantifying 24-hour reactions by change in ear thickness. SE or methylated bovine serum albumin was used to sensitize and challenge mice for delayed-type hypersensitivity (DTH) reactions which were quantified at 24 h by change in foot pad or ear thickness. CS and DTH reactions of W/Wv and LM mice were similar. No evidence of immune deficiency of W/Wv mice was found.
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PMID:Immune response potential of mast cell-deficient W/Wv mice. 351 77

Twenty-one parasite-naive dogs were infected with 60,000 protoscolices of Echinococcus granulosus. Transformation of peripheral lymphocytes was investigated before and 29 days after the infection, immunoglobulin concentration and anti-hydatid fluid protein (HFP) titers in serum and feces before and at 35 days of infection, skin reactivity to HFP at 36 days, and characteristics of the parasites at 40 days. The infection caused a significant depression of the spontaneous, lipopolysaccharide-stimulated, and purified protein derivative-stimulated blastogenesis. Responses to phytohemagglutinin were unchanged and reactivity to concanavalin A was enhanced with the infection. Only the concentrations of IgG and IgA in the serum and IgA in the feces increased significantly after infection. Fifteen (71%) dogs produced significant serum titers of anti-HFP hemagglutinins but copro-antibodies were detectable in only 3 dogs at minimum titers. Titers were abolished by treatment with 2-mercaptoethanol. The serum of 11 (52%) dogs transferred passive cutaneous anaphylaxis to guinea pigs but none transferred skin reactivity to pups or rabbits. Five and 1 (but not 0.2) micrograms of HFP caused skin reactivity in 4 parasite-naive dogs. Nineteen (90.5%) infected dogs reacted significantly to skin inoculation of 0.2 microgram of HFP at 0.5 hours and 13 (62%) at 6 hours. The 7 dogs with the highest anti-HFP serum titers or the greatest skin reactivity at 6 hours had significantly less mature or fewer tissue parasites, respectively, than the 7 dogs with the smallest responses. Since there was evidence that the specific immunity was still developing at the time of the study, these results indicate that immunological diagnosis of, and artificial immunization against, canine echinococcosis are feasible.
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PMID:Humoral immunity in the prepatent primary infection of dogs with Echinococcus granulosus. 352 Oct 67

The effect of dermonecrotic toxin (DNT), fimbrial hemagglutinin (FHA), K-agglutinogen, lipopolysaccharide (LPS), and pertussigen from Bordetella pertussis on the production of IgE and IgG1 antibodies to hen egg albumin (Ea) was investigated in C57BL/6 mice. The IgE antibody contents were determined by passive cutaneous anaphylaxis (PCA) in the skin of Lewis rats, while the IgG1 antibody contents were determined by PCA reactions on the skin of mice using sera that had been heated for 3 hr at 56 C to destroy the IgE antibodies. Among the B. pertussis components tested, pertussigen was the most effective adjuvant for increasing the IgE and IgG1 antibodies to Ea. LPS also moderately increased both types of antibodies, and FHA slightly increased the IgG1 titers. When LPS was given 5 days before Ea, it suppressed both IgE and IgG1 titers while FHA had only slight adjuvant action on both type of antibodies. When each of the components was tested for its ability to modify the adjuvant action of pertussigen, it was found that only DNT interfered significantly with the adjuvanticity of pertussigen when given on the day of immunization with Ea. When the components were given 5 days before Ea, DNT produced significant suppression of only the IgG1 response. LPS, FHA, and K-agglutinogen did not significantly affect the adjuvant action of pertussigen.
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PMID:Effects of Bordetella pertussis components on IgE and IgG1 responses. 632 10

The ocular immediate hypersensitivity reaction in guinea pigs to topically applied normal rabbit serum can be evoked as long as 4 years after sensitization. The reaction was as severe and tended to persist for longer than that evoked 6 months after sensitization. Passive cutaneous anaphylaxis tests showed that very high titres of homocytotropic antibodies were present and that both IgE- and IgG1-like antibodies were involved. Sensitization with one set of injections instead of two was not consistently successful and the response on challenge was mild to moderate. Pretreatment of eyes with Isoptocarpine before antigenic challenge had no effect on the response. The addition of bacterial lipopolysaccharide to the first set of sensitizing injections produced hypersensitivity in animals which were otherwise refractory to sensitization.
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PMID:Immediate hypersensitivity in the guinea pig conjunctiva. III. long-term persistence of the hypersensitive state and characterization of antibodies. 701 38


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