The effect of DEAE dextran, dextran sulfate and dextran on porcine mixed lymphocyte reaction.
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Animals↗
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Isotypes of antibodies induced by plain dextran or a dextran-protein conjugate.
Mice were immunized with alpha (1----6) dextran or its protein conjugate with monthly intervals, and their antibodies were quantitated with an isotype-resolved radioimmunoassay. Plain dextran (molecular weight = 5-40 million) induced antibody concentrations varying from 20 to 80 micrograms/ml (primary response). The response to a booster injection was weaker than the response to the first injection. More than 90% of anti-dextran antibodies were IgM but IgG and IgA responses could be unequivocally demonstrated. IgG1 and IgG3 were the predominant subclasses of IgG. Dextran antibody responses to a conjugate of dextran (molecular weight approximately equal to 10000) and chicken serum albumin (CSA) were stronger (80-300 micrograms/ml) than responses to plain dextran, and anti-CSA responses to the conjugate were even stronger (up to 900 micrograms/ml). Three distinctly different isotype patterns were observed. A pattern IgM much greater than IgG1 = IgG3 greater than IgG2a prevailed in responses to the plain dextran and in primary anti-dextran responses to dextran-CSA. Another pattern IgG1 greater than IgG3 greater than IgM greater than IgG2a was observed in late anti-dextran responses to dextran-CSA. The third pattern IgG1 much greater than IgG2a greater than IgG3 approximately equal to IgM was characteristic of anti-CSA antibodies. Little IgG2b or IgA antibodies were found. Different isotype patterns can best be explained on the basis of secondary factors such as T cell help.
Animals↗
Thromboembolism following total hip-replacement arthroplasty. The efficicy of dextran-aspirin and dextran-warfarin in prophylaxis.
The efficacy of two antithrombotic regimens, combined dextran and aspirin and combined dextran and warfarin, was analyzed by comparing the incidence of thromboembolism following total hip replacement in two groups of similar patients. Of the 427 who received dextran and aspirin, 7 per cent had thromboembolic complications, including one case of fatal pulmonary embolus and one case of recurrent emboli that required vena caval ligation, and 15 per cent had wound-healing complications. Of the 197 patients who received dextran and warfarin, 5 per cent had thromboembolism and 24 per cent had wound healing complications. Although both prophylactic regimens seemed effective, dextran and aspirin appeared less effective in reducing thromboembolic complications than dextran and warfarin, but there were fewer wound complications in that group. One-fourth of the patients on dextran-warfarin were not adequately anticoagulated despite close supervision. In forty-five patients with a history of thromboembolism who were excluded from the study and analyzed separately, warfarin alone and the two described regimens were equally ineffective in preventing thromboembolism, and the incidence of thromboembolic complications was high. Dextran-aspirin and dextran-warfarin appear to be satisfactory and relatively simple methods of thromboembolic prophylaxis.
Arthroplasty↗
The mechanism of dextransucrase action. Activation of dextransucrase from Streptococcus mutans OMZ 176 by dextran and modified dextran and the nonexistence of the primar requirement for the synthesis of dextran.
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Arthrobacter↗
Plasma volume after dextran infusion in rats sensitive and non-sensitive to dextran.
Plasma volume determinations were done with RIHSA under normal conditions and after intravenous infusion of dextran solutions. The plasma volume of normal rats in millilitre was found to be 0.026 X body weight + 0.92. Infusion of dextran into dextran-sensitive Sprague-Dawley rats was followed by a marked plasma volume reduction and haemoconcentration as consequence of an anaphylactoid reaction. This reaction could be partially inhibited by pretreatment with cyproheptadine chloride. Plasma volume determination with the method used in this study can be used to evaluate the dextran-anaphylactoid reaction. In dextran non-sensitive Wistar rats, infusion of dextran had a strong plasma volume-expanding effect comparable to the plasma volume-expanding effect of dextran in humans. No signs of abnormal leakage of fluid out into the extravascular space were evident, which indicated that the Wistar rats really were non-sensitive to dextran.
Animals↗
Effect of substitution on reactivity of B 512 dextran fractions with anti-B 512 dextran in heterologous passive cutaneous anaphylaxis.
The influence of type and degree of substitution of B 512 dextran fractions on reactivity with rabbit antibodies against unmodified B 512 dextran was studied on heterologous passive cutaneous anaphylaxis in guinea pigs. Low degrees of substitution, i.e. 1 substituent group per 7-30 glucose residues, affected reactivity with anti-dextran only slightly or not at all. This was shown for the following substituents: sulphate, carboxymethyl, phosphate, diethylaminoethyl, hydroxypropyl, butyryl, caprylyl, stearoyl, and fluoresceinoyl groups. With high degress of substitution, i.e. 1-3 substituents per 2 glucose residues, reactivity with anti-B-512-dextran is completely abolished for some substituents, and a new immunological identity conferred on the substituted dextran. Stongly charged groups like sulphate, carboxymethyl and diethylaminoethyl abolish reactivity with anti-B-512-dextran at relatively lower degrees of substitution than more neutral groups like methyl and acetyl. The anti-B-512-dextran represents a specific reagent for alpha-1,6-linked polyglucose, as evidenced by complete cross-reactivity with synthetic linear dextran; its specificity is emphasized by non-reactivity with alpha-1,6-linked synthetic manna, the monomeric residues of the two polymers differing only in position of the C-2 hydroxyl groups.
Animals↗
Dextran-induced anaphylactoid reactions in man: role of dextran reactive antibodies.
Dextran reactive antibodies (DRA) were studied in 123 patients having experienced dextran-induced anaphylactoid reactions (DIAR) during 1970-1975. No evidence for reaginic DRA was obtained by radioallergosorbent technique and passive cutaneous anaphylaxis in Cynomolgus monkeys; total IgE levels were within normal range. It is concluded that DIAR are not mediated by dextran-specific reagins. Further, no reaginic antibodies against potential contaminants from the dextran manufacturing process were demonstrable. In two population samples of normal human sera from Sweden and Germany hemagglutinating DRA (IgG, IgA, and IgM classes) were found in 63 and 74%, high titres (16-256) comprising 14 and 25%. In dextran reactors a direct positive correlation between titres of hemagglutinating DRA and increasing severity of DIAR was observed. The accumulation of high DRA titres in severe reactions may be taken as circumstantial evidence for the causal role of hemagglutinating DRA in these cases. However, if high titres of DRA alone were responsible for triggering DIAR, the expected frequency would be more than thousand times higher than the reported global incidence of DIAR. To explain this discrepancy, involvement of certain Ig classes or subgroups, possibly in combination with other predisposing factors is suggested. In mild reactions DRA appear to play a negligible role. Positive dextran wheal and flare reactions, often correlated with high titres of hemagglutinating DRA, were seen in 32% of dextran reactors, indicating that skin tests are of limited predictive value. No significant difference between sexes, age groups, or pre- and intraoperatively started dextran infusions was observed; association with certain diseases was not apparent.
Adolescent↗
Dextran antibodies, complement conversion and circulating immune complexes after intravenous iron dextran therapy in dialysed patients.
Serum immune complexes, plasma dextran antibodies and percentage conversion of complement have been measured in 20 dialysed patients before and after an intravenous infusion of iron dextran providing 600 mg elemental iron. Complement conversion was unmeasurable and there were no changes in circulating immune complexes. The presence of dextran antibodies in nine patients before the infusion was not related to prior exposure to iron dextran. They became undetectable in these patients within hours after the infusion, reappearing 1 month later in three. Two of three patients reporting mild aches and shivers on the day following the infusion had no detectable dextran antibodies. An adverse reaction involving inflamed joints occurred 1-2 days after a second infusion given to one of the patients studied above. The parameters under study were again measured and did not appear to relate to the reaction. The presence of dextran antibodies does not preclude the giving of iron dextran to patients on dialysis, and the immune complex and complement systems remain undisturbed by iron dextran infusions.
Adolescent↗
Mechanisms of B cell tolerance. I. Tolerance to dextran B1355 induced with the oxidized dextran.
The bacterial dextran B1355, which is normally a potent thymus-independent immunogen, was made tolerogenic by oxidation. The injection of the oxidized dextran into BALB/c mice before, at the same time, or up to 4 days after the injection of the immunogenic form of the dextran resulted in a marked immunologically specific suppression of the number of anti-dextran antibody-forming cells found in the spleen. This suppression resulted from a direct inactivation of antibody-forming cell precursors rather than from either inhibition of antibody secretion or the exhaustive utilization of precursor B cells that have been observed in other tolerance systems. A substantial degree of tolerance was achieved after only a 1-hr in vivo exposure of the spleen cells to the tolerogen. At a dose of 1 mg of oxidized dextran per mouse, tolerance persised for at least 3 weeks. A complete recovery was apparent by 10 weeks. The stability of the tolerance was demonstrated by transferring tolerant spleen cells to irradiated recipients. The response in the recipient animals to an immunogenic dextran challenge remained suppressed. It appears that the tolerogenicity of the oxidized dextran is due to its ability to couple covalently with free amino groups in or near the receptor site of the cell membrane via the reactive dialdehyde groups of the dextran.
Animals↗
Immunological unresponsiveness to native dextran B512 in young animals of dextran high responder strains is due to lack of Ig receptors expression. Evidence for a nonrandom expression of V-genes.
Young mice of dextran high responder strains were found to be complete nonresponders to the alpha-1-6 epitope of dextran during 30-40 days after birth. They also failed to respond to thymus-dependent dextran-protein conjugates. Cells from young and adult mice were activated equally well to polyclonal antibody synthesis by the polyclonal B-cell-activating property of dextran. There was no age difference in the immune response to haptens conjugated to dextran, indicating that dextran can function as an efficient carrier also in young mice. Unresponsiveness could not be attributed to suppressor T cells or to a suppressive environment in young animals, as shown by transfer experiments, in which living or irradiated cells from young and adult mice were admixed in various ways and transferred to irradiated recipients of different ages. Cells from young mice did not affect response of adult cells (and the reverse), nor did the age of the irradiated recipient influence the response. When lymphocytes from young and adult mice were polyclonally activated in vitro by lipopolysaccharide, only cells from young mice failed to synthesize antibodies against the alpha-1-6 epitope of dextran, although they produced antibodies of all other specificities tested for. It was concluded that young animals fail to express immunoglobulins directed against the alpha-1-6 epitope during the first 30-40 days after birth. Since the mice possess the VH gene coding for antibodies against this particular epitope, it was concluded that the timing of V gene expression is regulated during development, possibly at the V-C gene translocation level.
Aging↗
Anti-human immunodeficiency virus effects of dextran sulfate are strain dependent and synergistic or antagonistic when dextran sulfate is given in combination with dideoxynucleosides.
The effects of three molecular weight ranges of dextran sulfate on five different human immunodeficiency virus (HIV) isolates (from patients with acquired immunodeficiency syndrome), alone and in combination with dideoxynucleosides, were investigated in vitro. The higher the molecular weight range of dextran sulfate, the more potent the activity as assessed by a quantitative syncytium formation assay. Although all five HIV isolates had similar susceptibilities to the inhibitory effects of dideoxynucleosides, the two clinical isolates of HIV (HIV type 1 [HIV-1] TM and SP) exhibited a pattern of reduced susceptibility to dextran sulfate when compared with the two cloned isolates (HIV-1 WMF and HIV-2 ROD) and a prototype laboratory strain (HIV-1 IIIB). In combination with dideoxynucleosides, the high-molecular-weight range of dextran sulfate (500,000) resulted in an antagonistic response directed against the two clinical isolates of HIV (HIV-1 TM and SP) when the antiviral concentrations of dextran sulfate were in the ineffective range. Additive or synergistic effects were seen with the other three HIV isolates and all five HIV isolates when the low-molecular-weight range of dextran sulfate (8,000) was used. The results of these studies raise issues on the impact of drug-resistant strains on disease progression and the use of dextran sulfate in combination with nucleoside analogs for the clinical management of HIV disease.
Cells, Cultured↗
Permeability of renal peritubular capillaries to neutral dextrans dextrans and endogenous albumin.
Renal lymph-to-renal vein concentration ratios (CL/CV) for neutral dextrans (18-42 A effective radii) and endogenous serum albumin were measured in rats before and during acute colume expansion with isoncotic plasma or Ringer solution. Under all conditions studied, CL/CV decreased with increasing dextran size, in normal hydropenia falling from 0.93 +/- 0.03 SE at 18 A to 0.24 +/- 0.02 a 42 A (n = 12). Albumin (36 A pradius) behaved in a manner similar to a 40 A dextran, CL/CV averaging 0.33 +/- 0.03 (n = 12) in hydropenia. For all dextran sizes studied and for albumin, CL/CV decreased markedly during either form of volume expansion. Ringer loading produced significantly greater decreases in CL/CV for the larger dextrans and albumin than did plasma loading, and also resulted in much greater increases in renal lymph flow, while causing increases in whole kidney fluid reabsorption similar to those with plasma loading. With a compartmental model in which diffusion of dextrans and albumin from capillary lumen to interstitium is opposed by capillary uptake of tubule reabsorbate, these results are interpreted to indicate that connective reflection coefficients for dextrans with radii great than or equal to 36 A and albumin are essentially equal to 1. Indirect evidence is therefore provided that albumin and the larger globulins exert their full osmotic pressures across the walls of peritubular capillaries.
Animals↗
A comparison of the anaphylactoid actions of a synthetic linear dextran and a natural branched dextran.
Synthetic linear dextran of molecular weight 40,000 produces the systemic anaphylactoid reaction in rats although it is about 4 times less active than the natural branched dextran of similar molecular weight. Similarly, it is less active on local injection into the foot or skin. However, in rats which have been bred for non-reactivity to systemic dextran, it is more active on local injection, resembling the activity of a branched natural dextran of much lower molecular weight (6,000). In human skin, the synthetic linear 40,000 sample is also more active than the natural branched sample of similar molecular weight in producing a wheal and erythema. The results suggest that the dextran receptor in the skin of man may be similar to that in rats genetically resistant to systemic dextran.
Anaphylaxis↗
[Randomized double-blind study of therapy of sudden deafness. Low molecular weight dextran + naftidrofuryl vs. low molecular weight dextran + placebo].
Eighty patients with idiopathic sudden deafness existing no longer than 10 days were included in a prospective randomized double-blind study. Patients were treated for 10 days with infusions of either 10% low-molecular weight dextran or the combination of low-molecular weight dextran with naftidrofuryl. Before treatment and after 10 days hearing loss in the affected ear was determined at 0.5, 1, 2, 3, 4 and 6 kHz. The mean hearing loss was then calculated as the average from these values. During monotherapy with low-molecular weight dextran the mean hearing loss decreased from 40 to 27 dB compared to 38 to 17 dB when naftidrofuryl treatment was added (p < 0.01 between groups). A significant benefit of naftidrofuryl on hearing loss was also found at frequencies between 0.5 and 3 kHz. Furthermore, patients reported better improvement of tinnitus when naftidrofuryl was combined with dextran. Two patients receiving dextran alone developed side effects: one had an allergic reaction causing withdrawal of treatment, which the other case had vertigo, nausea and headache with spontaneous recovery. The results of the study showed that treatment with naftidrofuryl in addition to hemodilution with low-molecular weight dextran was of therapeutic benefit in the therapy of sudden deafness without increasing the rate of side effects.
Administration, Oral↗
Heparin, dextran 1000 and metastasis formation after I.V. tumour cell injection in dextran non-sensitive rats.
The present study of the effect of heparin and dextran 1000 on the metastasis formation after i.v. tumour cell injection in dextran non-sensitive rats using a syngeneic 20-methylcholanthrene induced fibrosarcoma showed that heparin treatment decreased with formation of pulmonary metastases in animals both untreated and treated with dextran 1000. Treatment with dextran 1000 increased the formation of pulmonary metastases in animals both untreated and treated with heparin and the effect of dextran 1000 was thus not affected by heparin treatment. Heparin did not have any direct action on the tumour cells, which influenced metastasis formation. The data suggest that heparin acts as an anticoagulant with decreased microthrombus formation around lodged cells and that dextrax 1000 stimulates metastasis formation primarily by mechanisms other than intravascular coagulation.
Animals↗
Destruction of dextran-coated target cells by normal human lymphocytes and monocytes. Induction by a human anti-dextran serum with IgG antibodies restricted to the IgG2 subclass.
A human anti-dextran serum, EAK, with IgG antibodies restricted to subclass IgG2, was tested for its capacity to induce lysis of dextran-coated chicken erythrocytes by normal human lymphocytes or monocytes. Another human anti-dextran serum, RGM, with most antibodies belonging to sublass IgG1, and a hyperimmune rabbit anti-dextran serum were used for reference. In lymphocyte-mediated erythrolysis, serum EAK gave rise to 51-Cr release varying from 20% to 80% in different experiments. The hyperimmune rabbit serum was 100 to 1000 times more active, whereas serum RGM was consistently negative. These results correlated well with the concentration of anti-dextran antibodies in these sera. In monocyte-mediated erythrolysis serum EAK had a somewhat higher titer than in lymphocyte-mediated lysis, and serum RGM had a weak but significant activity at low dilutions. Serum EAK also induced erythrophagocytosis by monocytes. Ultracentrifugation did not significantly decrease the inductive capacity of this serum. The results show that antibodies of human sublass IgG2 are efficient inducers of effector functions in both lymphocytic and monocytic cells. Myeloma proteins of the four IgG subclasses were tested for inhibitory capacity in lymphocyte- or monocyte-mediated erythrolysis. Either serum EAK or the rabbit reference serum was used for induction of erythrolysis. Individual myeloma proteins within and between the subclasses varied considerably in inhibitory power. However, whereas IgG1, IgG2, and IgG3 proteins inhibited lymphocyte-mediated erythrolysis induced by either type of antiserum, the two IgG4 proteins tested were essentially negative. These results suggest a lack of specificity of the Fc receptor for subclasses IgG1, IgG2, and IgG3 in both heterologous and homologous inhibition. In monocyte-mediated erythrolysis, IgG1 and IgG3 were strong inhibitors, whereas inhibition by IgG2 and IgG4 was weak and inconsistent. This pattern was seen regardless of whether and inducing antiserum was of rabbit or human origin. Similar results were obtained in monocyte-induced erythrophagocytosis induced by serum EAK. These and previous results suggest that effector cells of the lymphocytic (K cell) variety have Fc receptors different from those of monocytic cells. However, the basis for the differences observed in the inhibition tests remains to be elucidated.
Animals↗
Dextran-mediated interbacterial aggregation between dextran-synthesizing streptococci and Actinomyces viscosus.
Streptococcus sanguis and Streptococcus mutans bind to the surface of Actinomyces viscosus, producing large microbial aggregates. Aggregates form rapidly and are not easily dissociated by vigorous mixing. The binding is mediated by dextran. Glucose-grown streptococci will not aggregate unless they are first mixed with high-molecular-weight dextran. Aggregation is induced with dextrans isolated from Leuconostoc, S. sanguis, or S. mutans. Sucrose-grown streptococci will adhere to A. viscosus without the addition of an exogenous source of dextran. A. viscosus will bind dextran and then bind glucose-grown streptococci. Aggregation occurs over a wide pH range and is dependent on cations. The aggregating activity of A. viscosus is both protease and heat sensitive. The aggregating activity of S. sanguis is heat stable but sensitive to dextranase.
Actinomyces↗
Dextrans and the formation of pulmonary metastases after intravenous tumour cell injection in rats non-sensitive to dextran.
This study showed, that in a syngeneic tumour-host system in rats non-sensitive to dextran, dextran 40 and dextran 100 did not stimulate metastasis formation after intravenous tumour cell injection, neither when given as intravenous pretreatment nor when given in the tumour cell suspension. Dextran 1000 stimulated the formation of metastases in both these situations. Disturbed microcirculation, intravascular coagulation and effects upon the tumour cell membrane appear to be the main resons, why dextran 1000 stimulated metastasis formation under the experimental conditions used.
Animals↗