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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Extracts of Brucella abortus 2308S, prepared either by aqueous extraction of sonically ruptured cells or by phenol-water extraction of whole cells, were subjected to various fractionation procedures and then analyzed to determine their immunoelectrophoretic patterns and chemical properties. Fraction A, prepared from sonic extracts, contained at least nine precipitable components when analyzed by immunoelectrophoresis. Of these, five components gave reactions of nonidentity with each other and, hence, represented separate antigens having unrelated determinant groups. Antigenic component IX, found in both the phenol and sonic extracts, did not form a precipitin line in the presence of serum that had been adsorbed with whole cells and was therefore tentatively identified as a "surface" antigen. From several lines of evidence, component IX was thought to be a lipopolysaccharide similar to the AP substance described by Miles and Pirie and shown by them to carry the "abortus" and "melitensis" determinant groups.
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PMID:Antigens of Brucella abortus. I. Chemical and immunoelectrophoretic characterization. 496 Jan 79

Cyclosporin A, an immunosuppressive peptide of fungal origin, was believed to selectively affect T lymphocyte functions and to have minimal affects on B lymphocytes. This study shows that, in the mouse, T-dependent B cells and those responding to certain T-independent antigens (so-called TI-1 antigens) are indeed resistant to the drug. However, B cells responsive to other TI antigens (TI-2) are exquisitely sensitive. Thus, doses of the drug that completely abrogate responses to dinitrophenylated (DNP) Ficoll or dextran enhance the response to DNP-lipopolysaccharide and have minimal effects on the response to DNP-Brucella abortus. Virgin T helper cells are sensitive to the drug, whereas primed T cells are not. Cyclosporin A sensitivity therefore represents a novel marker of functional B cell subsets in the mouse and presumably points to fundamental physiologic differences between such subsets.
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PMID:Selective effects of cyclosporin A on functional B cell subsets in the mouse. 615 10

The effect of the X-linked CBA/N genetic defect on the ability of mice to generate primary responses to thymic-dependent and thymic-independent antigens was assessed by comparing the ability of abnormal (CBA/N x DBA/2)F1 male mice and normal (DBA/2 x CBA/N)F1 male mice to generate 2,4,6-trinitrophenyl (TNP)-specific plaque-forming cell responses to TNP-keyhole limpet hemocyanin (KLH), TNP-conjugated Ficoll (TNP-Ficoll), TNP-Brucella abortus (BA), and TNP-lipopolysaccharide (LPS). The reciprocal F1 combinations used in this study differ genetically only in the origin of their X chromosome, but differ immunologically in that (CBA/N x DBA/2)F1 male mice express all the CBA/N immune abnormalities, whereas (DBA/2 x CBA/N)F1 male mice are immunologically normal. Analysis of thymic-dependent responses to TNP-KLH revealed that abnormal F1 mice were capable of generating primary responses in vivo to high doses of TNP-KLH, but failed to generate responses to suboptimal doses of TNP-KLH that were still immunogenic for normal F1 mice. Furthermore, under limiting in vitro micro-culture conditions, the abnormal F1 mice failed to generate primary thymic-dependent responses to any dose of TNP-KLH, even though under the identical conditions normal F1 mice consistently responded to a wide antigen dose range. The cellular basis of the failure of abnormal F1 mice to respond in vitro to TNP-KLH was investigated by assaying the ability of purified populations of accessory cells, T cells, and B cells from these mice to function in responses to TNP-KLH. The results of these experiments demonstrated that helper T cells and antigen-presenting accessory cells from abnormal F1 mice were competent and functioned as well as the equivalent cell populations from normal F1 mice. Instead, the failure of CBA/N mice to generate primary in vitro responses to TNP-KLH was solely the result of a defect in their B cell population such that B cells from these mice failed to be triggered by competent helper T cells and/or competent accessory cells. Similarly, the failure of abnormal F1 mice to respond either in vivo or in vitro to TNP-Ficoll was not the result of defective accessory cell presentation of TNP-Ficoll, but was the result of the failure of B cells from these mice to be activated by competent TNP-Ficoll-presenting accessory cells. In contrast to the failure of B cells from abnormal F1 mice to be activated in vitro in response to either TNP-KLH or TNP-Ficoll, B cells from abnormal F1 mice were triggered to respond to TNP-BA and TNP-LPS, antigens that did not require accessory cell presentation. The specific failure of B cells fron abnormal F1 mice to be activated in responses that required antigen-presentation by accessory cells suggested the possibility that the X-linked CBA/N genetic defect resulted in B cell populations that might be deficient in their ability to interact with antigen-presenting accessory cells...
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PMID:Role of accessory cells in B cell activation. III. Cellular analysis of primary immune response deficits in CBA/N mice: presence of an accessory cell-B cell interaction defect. 615 44

Purified lipopolysaccharide (LPS) extracted with phenol-water from smooth Brucella abortus was hydrolyzed with 1% acetic acid at 100 degrees C. The degraded polysaccharide (AH) released gave reactions of identity with the native polysaccharide hapten (NH) in phenol-water- or trichloroacetic acid-extracted endotoxin preparations of B. abortus and with the polysaccharide (poly B) extracted by trichloroacetic acid from rough B. melitensis strain B115. Poly B was present in the soluble cytoplasmic fraction but not in the membrane fraction, of disrupted B115 cells. It could not be extracted from three rough mutants of B. abortus or from B canis or B. ovis cells. Both AH and NH shared determinants present on smooth LPS and missing from poly B. Sugars found in purified LPS, NH, and AH included mannose, glucose, quinovosamine, glucosamine, and 2-keto-3-deoxyoctonate. Poly B contained only a trace amount of quinovosamine and no 2-keto-3-deoxyoctonate detectable by the thiobarbiturate assay. Sera from some rabbits immunized with pure smooth LPS and some, but not all, cows infected with field strains of B. abortus recognized the determinants missing from poly B. A subclass-specific enzyme-linked immunoassay showed that most of the antibody in sera from infected cows which binds to smooth LPS and to NH is of the immunoglobulin G1 subclass.
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PMID:Immunochemical characterization of Brucella lipopolysaccharides and polysaccharides. 616 16

An enzyme immunoassay, with phenol-water extracted lipopolysaccharide (LPS) from Brucella abortus as antigen, was used to detect the class-specific antibody response in sera from 173 patients with B. abortus, B. melitensis or B. suis infection. Sera from 30 patients with salmonellosis, yersiniosis or tularaemia and from 25 healthy individuals served as controls. The B. abortus LPS antigen permitted a safe diagnosis of acute and chronic brucellosis with high IgM and rising IgG titres in sera collected in the acute stage of the disease, and with elevated IgG titres only in the chronic stage. The B. abortus LPS antigen also permitted a specific diagnosis with the exception of the high titres estimated in sera from patients with Yersinia enterocolitica 09 infection. The problem with that well-known reciprocal cross-reactivity was overcome by using two additional antigens: Y. enterocolitica 09 native and periodate oxidized and borohydride reduced LPS preparations. In sera from patients with brucellosis high titres were estimated against all three antigens, whereas in sera from patients with yersiniosis caused by serotype 09 high titres were measurable only with the B. abortus and the Y. enterocolitica native LPS antigens. These data suggest that the B. abortus and Y. enterocolitica 09 LPS share one antigenic determinant resistant to periodate oxidation and borohydride reduction, and that in addition the Y. enterocolitica 09 LPS has a determinant which is sensitive to periodate oxidation and borohydride reduction.
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PMID:Enzyme immunoassay of the antibody response to Brucella and Yersinia enterocolitica 09 infections in humans. 617 1

We investigated whether the definition of functional B cell subpopulations changes after the exposure of B cells to specific antigen. Recent in vivo priming with fluorescein- (FL) coupled T-independent (TI) antigens leads to an augmentation of the subsequent in vitro responses of B cells to FL-coupled TI antigens, including FL-polymerized flagellin, FL-lipopolysaccharide, and FL-Brucella abortus, as well as a FL-coupled T-dependent (TD) antigen, FL-keyhole limpet hemocyanin (KLH). This effect, which is evident 7 days after priming, is of short duration in that B cells from FL-Ficoll injected mice display normal responsiveness 3 wk after priming. When mice are primed with FL-KLH, the TD antigen, B cells responsive to a subsequent FL-KLH challenge are expanded, but not short-term cross-priming for any of the TI antigen challenges is observed. Limiting dilution precursor analysis shows that B cell populations responding to different FL-coupled TD and TI antigens overlap in unimmunized animals. FL-TI antigen priming induces not only quantitative changes in the responding B cells (increased precursor frequencies) but also results in functional changes in FL-specific B cells. The primed B cells now respond to FL-hapten in a carrier-restricted manner and behave as independent (non-overlapping) subpopulations. We suggest that B cell responses to different forms of the same hapten are influenced in part by their recent "history" of antigenic exposure.
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PMID:Effect of recent antigen exposure on the functional expression of B cell subpopulations. 617 88

Two different cross-reactive idiotype (CRI) groups are distinguishable in the Ab response of A/J mice to the p-azobenzenearsonate (ABA) hapten: CRIA and CRIm. These two groups showed distinct patterns of relative dominance in the ensuing response depending on whether the inducing Ag was a T cell-dependent (TD) form of ABA, such as ABA-KLH or ABA-CGG, or a T-independent type 1 (TI-1) form, such as ABA-Brucella abortus or ABA-lipopolysaccharide (LPS), and on whether the response was elicited in vivo or in vitro. The CRI+ component of primary in vivo plaque-forming cell (PFC) responses to TD ABA Ags was largely (greater than 90%) CRIA+ as was, to a slightly lesser extent (greater than 75%) the CRI+ portion of secondary or hyperimmune serum Ab or PFC responses to the same Ags. In contrast, in vivo primary and hyperimmune PFC responses to ABA-Bru or ABA-LPS showed a significantly lower CRIA/CRI ratio, averaging 0.5-0.6, with some individual mice giving figures as low as 0.2, indicating predominance of CRIm over CRIA. Serological analysis of hyperimmune anti-ABA Abs from a group of 5 A/J mice immunized with ABA-Bru gave a figure of less than 0.5 for the CRIA/CRI ratio. The most striking disparity from the TD pattern was seen in primary in vitro PFC responses to the TI ABA Ags; here ratios of less than 0.2 were generally seen. Since T cell removal did not alter the Id pattern in the TI responses, CRIA-specific Ts cells do not account for the weak expression of CRIA in such responses. We propose a model that explains these results on the basis of differential expression of IdX dominance by two distinct B cell subpopulations--equatable to the Lyb-5+ and Lyb-5- B cell subsets--along with differential relative activation of these subsets in different types of responses. Examination of anti-ABA PFC responses of F1 progeny of CBA/N and A/J mice to ABA-Bru lends support to this hypothesis since CRIA expression was significantly lower in mice with the xid defect.
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PMID:Idiotype profile of an immune response. II. Reversal of the relative dominance of major and minor cross-reactive idiotypes in arsonate-specific T-independent responses. 619 21

Four supposedly T-independent antigens, fluorescein (FLU)-E. coli lipopolysaccharide (LPS), FLU-Brucella abortus (FLU-BA), FLU-Ficoll, and FLU-polymerized flagellin (FLU-POL), were tested for their capacity to stimulate B cell proliferation and antibody formation. Single, isolated FLU-specific adult murine splenic B lymphocytes were used as the unequivocal target cell in 10-microliter cultures unsupported by accessory, feeder or filler cells. The stimulatory capacity of four supposed mitogens, LPS, dextran sulfate (DXS), BA, and Ficoll, and of one T-dependent antigen, FLU-keyhole limpet hemocyanin (FLU-KLH), was also studied. Stimuli were used over a wide range of concentrations with or without added T cell-derived, antigen-nonspecific factors promoting B cell growth and differentiation (BGDA). The results allowed triggering stimuli to be divided into four groups: 1) FLU-KLH failed to stimulate single B cells even in the presence of BGDA as did unconjugated Ficoll; 2) FLU-POL was stimulatory only when BGDA was also present, as was unconjugated BA; 3) FLU-BA was slightly stimulatory in the absence of BGDA, but much more so in the presence of BGDA, as was a low concentration of LPS; 4) FLU-LPS and FLU-Ficoll were powerfully stimulatory over a 100,000-fold range of concentrations, and at no concentration did BGDA affect their capacity. LPS or LPS + DXS at high concentrations behaved similarly. The differing behavior of the various conjugates did not correlate either with their supposed "TI-1" or "TI-2" status or with the mitogenic properties of the carrier portion of the antigen. For example, FLU-Ficoll at 0.01 microgram/ml caused 28% of FLU-specific B cells to form proliferating clones, 70% of which secreted immunoglobulin, but a 1000-fold higher concentration of Ficoll failed to stimulate single cells. It is tempting to regard stimuli in group 4 as truly T-independent. However, the intentional addition of thymus filler cells to single B cells triggered by these agents markedly raised antibody formation. Until the nature of this further "helper" effect is understood, it would be unwise to ignore the possibility that T cells or accessory cells are involved.
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PMID:A reappraisal of "T-independent" antigens. I. Effect of lymphokines on the response of single adult hapten-specific B lymphocytes. 619 7

Hybridomas producing antibodies to determinants associated with the lipopolysaccharide (LPS) of Brucella abortus and B melitensis were obtained by polyethylene glycol fusion of the SP2/0 myeloma cell line with B lymphocytes harvested from a Sprague-Dawley-derived rat previously immunized with whole B abortus strain 1119 organisms. Two clones, BRU38 and BRU28 , were selected for their ability to react with whole B abortus organisms and purified smooth-LPS ( f5p ). The BRU38 monoclonal antibodies were absorbed with live, rough strain 45/20 and smooth strains of B abortus and B melitensis organisms, whereas only smooth strains absorbed the antibody activity from BRU28 . Complete inhibition of the monoclonal's activity could be achieved with crude smooth-LPS, a purified f5p fraction, and a water-soluble acid degraded polysaccharide. Absorption of BRU38 and BRU28 with rough Brucella LPS, polysaccharide-B antigen, keto- deoxyoctanoic acid, or with several sugars and fatty acids known to be components of the Brucella LPS complex had no effect on the monoclonals. The data indicate that antigenic determinants are associated with the smooth LPS complex, probably with the O-side chain, and are expressed patchwise and in different quantities on several strains of B abortus and B melitensis. The B abortus rough strain 45/20 contains surface determinants which lead to the agglutination of smooth strain 1119 organisms. The potential use of monoclonals in competitive enzyme-linked immunosorbent assays for diagnostic purposes is discussed.
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PMID:Monoclonal antibodies to Brucella surface antigens associated with the smooth lipopolysaccharide complex. 620 43

Chickens were protected against fowl cholera by ribosomal vaccines prepared from noncapsulated Pasteurella multocida. Passive hemagglutination (PHA) titers to lipopolysaccharide (LPS) and the degree of protection conferred by ribosomal vaccines were diminished or abolished when ribosomes were chromatographed on an immunoadsorbent column. Addition of subimmunogenic amounts of serotype 1 (homologous) LPS to highly purified ribosomes resulted in vaccines that protected against challenge exposure and produced PHA titers to homologous LPS. Addition of serotype 5 LPS to highly purified ribosomes did not protect chickens against challenge exposure with serotype 1 P multocida, but produced PHA titers to serotype 5 LPS. Combinations of serotype 1 ribosomal RNA and serotype 1 (homologous) LPS did not protect chickens or produce PHA titers to LPS. Purified ribosomes from Brucella abortus, Aspergillus fumigatus, and chicken liver were combined with LPS from P multocida and were evaluated as vaccines. Brucella abortus and A fumigatus ribosomes combined with LPS protected chickens as well as did bacterin made from whole cells of P multocida. Chicken liver ribosomes combined with LPS did not provide protection. To determine whether a protein carrier would substitute for ribosomes, methylated bovine albumin (MBA) was combined with LPS and evaluated as a vaccine. A serologic response to LPS was induced by MBA-LPS vaccine, but the vaccine offered no better protection than when LPS was used alone as vaccine. Ribosome-LPS vaccines produced serologic responses to LPS that were at least 5-fold greater than those produced by MBA-LPS vaccine.
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PMID:Protection of chickens by ribosomal vaccines from Pasteurella multocida: dependence on homologous lipopolysaccharide. 620 28


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