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Results for “Dextrans”

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PubMed1983

New dextran derivatives. II. Preparation of compounds of copper (II) with 3-mercapto-2-hydroxypropyl ether of dextran.

The non-ionic compound of 3-mercapto-2-hydroxypropyl ether of dextran with cupric sulphide was obtained. The compound (called C-79) exhibited biological activity at parenteral administration to laboratory animals. The method of obtaining the compound as well as the properties of the latter were described. The results of gel chromatography suggested the existence of certain analogies with the known compounds of iron with dextran.

Animals↗

PubMed1988

xid mice fail to express an anti-dextran immune response but carry alpha(1-3)dextran-specific lymphocytes in their potential repertoire.

Even after repeated immunizations with alpha(1-3)dextran (Dex) male (CBA/N x BALB/c)F1 mice fail to produce specific antibodies whereas nondefective female littermates express an idiotype-positive anti-Dex immune response. This failure of xid mice to express serum anti-Dex immunoglobulins is not only limited to immunization with the thymus-independent (TI-2) antigen Dex, since immunization with anti-idiotypic antibodies against Dex-specific idiotypes does not overcome this defect. When xid lymphocytes are cultured in the presence of mitogens, in vitro anti-Dex responses are markedly reduced. We show here that alpha(1-3)Dex-specific hybridomas can be established by fusion of splenic lymphocytes from xid mice to Sp2/0 myeloma cells. Therefore, these mice do carry the potential to generate B cells specific for Dex. All hybridoma antibodies were found to be of IgM isotype, bearing the lambda light chain typical for alpha(1-3)Dex-specific antibodies. Whereas monoclonal anti-Dex antibodies obtained from spleen cell hybridomas from female littermates showed variable idiotope patterns, hybridoma proteins from the immune-defective NBF1-xid mouse expressed only a limited pattern of Dex-specific idiotopes, suggesting that these hybridomas derived from a common precursor.

Animals↗

PubMed1987

Regulation of the response to alpha(1-3) dextran: an anti-dextran associated idiotope of BALB/c mice is also expressed on A/J anti-NIP antibodies.

The functional properties of a mAb reactive to the B5 idiotope were analyzed in BALB/c, A/J and C.B20 mice. the B5 idiotope was specifically associated with the alpha(1-3) DEX response in a strain-specific manner in BALB/c mice (responder strain). It was serologically distinct from the previously described IdX idiotype and overlapped on part of the IdX+ and IdX- BALB/c anti-alpha(1-3) DEX response. While treatment of adult BALB/c mice with mAb B5 enhanced the serum anti-alpha(1-3) DEX antibody synthesis and induced de novo antibody synthesis in non-responder C.B20 mice, A/J non-responder mice remained unresponsive, despite elevated levels of serum B5+ dextran non-binding Ab3 immunoglobulins. However, in some of these A/J mice, we detected an enhancement of anti-NIP antibody synthesis. This anti-NIP antibody component was (1) specifically induced by mAb B5, (2) found in A/J, but not in BALB/c or C.B20 mice, and (3) specific towards the NIP hapten. These A/J anti-NIP antibodies bore either the lambda 1 or the kappa light chain and some of them also expressed the B5 idiotope. The B5 id thus appears as a typical id determinant shared by antibodies having different binding specificities, and it may have a role in the regulation of these responses.

Animals↗

PubMed1989

The immune response to bacterial dextrans. VI. No correlation between the frequency of cells expressing a major anti-dextran idiotype and the idiotype profiles of specific antibody responses.

C57BL/6 mice respond to Dextran B512 (Dex) with a predominant idiotype (Id) (17-9) while no such Id-positive antibodies are identified in the specific antibody response of BALB/c mice. We used limiting dilution systems to determine the absolute frequencies of clonal B-cell precursors producing the 17-9 Id in these two mouse strains and analysed the correlation between Id-expression and antibody activity at the clonal level. The results show very similar frequencies of anti-Dex and Id-positive B cells in both strains, but C57BL/6 mice contained fourfold higher frequencies of Dex-specific clonal precursors which are Id-positive. This kind of clone, although not used in the specific response of BALB/c mice, constitute roughly 20% of their anti-Dex repertoire and they are readily induced in this strain. Thus, immunization of both strains with anti-idiotypic antibodies results in the production of Id-positive anti-Dex antibodies with serum titres that directly correlate with precursor frequencies. The results show, therefore, that the section of clonal repertoires utilized in a primary immune response varies with the immunogen, even if thymus-independent. These observations are discussed in the context of the genetic controls of anti-Dex antibody responses and on the general question of the utilization of available antibody repertoires in immune responses.

Animals↗

PubMed1975

Interactions of the third component of complement (C3) with cross-linked dextran. III. Isolation and characterization of interacting components after enzymatic digestion of complement coated cross-linked dextran.

In previous investigations we could show that incubation of cross-linked dextran (Sephadex) with normal human and normal guinea pig serum results in the binding of C3 to Sephadex. This binding was found to be due to activation of C3 via an alternate pathway. In this paper data are presented which show that components bound to Sephadex can be recovered after enzymatic digestion of serum-reacted Sephadex beads. The digests were characterized with immuno-electrophoresis and double immunodiffusion techniques. It could be shown that the main component present in the digest was converted C3. Apart from C3 under our test conditions only minute amounts of C3A but no other serum proteins were detectable. The observation that almost exclusively C3 is bound to Sephadex is further supported by the finding that immunization of rabbits with serum-reacted Sephadex beads results in the exclusive formation of anti C3 antibodies. Implications from these findings and possible applications are discussed.

Antibody Formation↗

PubMedDate not supplied

DEAE-Dextran in the treatment of primary hypercholesterolemia and/or hypercholesterolemia combined with hypertriglyceridemia. A multicentric randomized study on the efficacy of DEAE-Dextran compared with Cholestyramine.

This study was carried out to verify the therapeutic homogeneity between DEAE-Dextran and Cholestyramine. Blood levels of total cholesterol, HDL, LDL and triglycerides were evaluated in 202 patients affected by dyslipidemia and treated with DEAD-D at 2.5 g/day or with Cholestyramine at 12 g/day for 30 days. At the end of treatment both drugs caused significant reduction of total cholesterol, LDL and triglycerides blood levels; DEAD-D was generally more effective than Cholestyramine, in particular on triglycerides values (30.6% and 13.7% of reduction respectively), and produced also a significant increase in HDL cholesterol, differently from Cholestyramine that was ineffective on this parameter.

Anticholesteremic Agents↗

PubMed2006

In vitro effects of dextran sulfate sodium on a Caco-2 cell line and plausible mechanisms for dextran sulfate sodium-induced colitis.

Pathogenic mechanisms responsible for inflammatory bowel disease (IBD) are poorly understood. In an IBD animal model, the oral administration of polysaccharides such as dextran sulfate sodium (DSS) induces colitis, which exhibit several clinical and histological features for IBD. However, pathogenic factors in the development of colitis remain unclear. Therefore, we investigated possible mechanisms for DSS-induced colitis, and mainly focused on biological responses from an intestinal epithelial cell line, Caco-2. Cytotoxicity and cytokine release were measured using MTS assays and ELISA, respectively. The effect of DSS on the transepithelial electrical resistance (TEER) of Caco-2 cell monolayers was also evaluated. Cell cycle progression was estimated using antibodies directed against p53 and cdc-2 proteins. The generation of reactive oxygen species (ROS) was measured using a DCFH-DA method. Pyridylamino-DSS (PA-DSS) was used as a fluorometric label in order to investigate fluorescence-microscopically the location of DSS in Caco-2 cells. DSS induced cytotoxicity on Caco-2 cells at 5%. DSS also induced strong TEER decrease at 3%. DSS induced the weak release of IL-8, IL-6, and TGF-beta1. Remarkably DSS arrested Caco-2 cell cycle and reduced the intracellular generation of ROS. Under fluorescence microscopy, PA-DSS entered cells and bound to the nucleus, indicating this binding of DSS may be involved in the cell cycle arrest of Caco-2 cells. The cell cycle arrest and reduced intracellular generation of ROS may be involved during initiation or throughout the early stages of DSS-induced colitis.

Caco-2 Cells↗

PubMed1975

Influence of molecular structure on the tolerogenicity of bacterial dextrans. II. The alpha1--3-linked epitope of dextran B1355.

Dextran B1355 is a branched glucose polymer containing 57 per cent alpha1--6, 35 per cent alpha1--3 and 8 per cent alpha1--2/1--4 linkages. Direct PFC responses to B1355 can be measured with sheep RBC sensitized with its O-stearoyl or palmitoyl derivative, and, as shown by inhibition analysis, are specific for an eptiope which is dependent on alpha1--3 linkages. B1355 is a potent immunogen in BALB/c mice producing peak PFC levels which approach 10(6) per spleen following an optimal dose of 1 mg. By contrast, the alpha-1--3-linked epitope of B1355 is feebly tolerogenic, for even 10 mg still induces a strong initial response. Mice given 1--10 mg sustain PFC levels 1--2 log10 above background for several months, but do not respond further to restimulation. Full recovery is attained by their spleen cells within 1 week of transfer into irradiated recipients. Deeper tolerance to this epitope was attained in vivo only when these larger doses of B1355 were injected during cyclophosphamide suppression. Two exceptions to this weak tolerogenicty were found. First, BALB/c spleen cells developed durable partial alpha1--3 tolerance following 2-hour incubation with B1355 in vitro. Second, CBA mice were fully tolerized by doses of 1 mg upwards. It is argued from these and other data in the accompanying papers that the relative resistance of BALB/c mice to induction of alpha1--3 tolerance is explicable neither as part of a more general phenomenon based on macrophage activity nor as due to an inadequate epitope density. A possible explanation based on features of the genetically determined high alpha1--3 responsiveness of BALB/c B cells is discussed.

Animals↗

PubMed1963