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PubMed1994

Human complement activation by polygeline and dextran 70.

The complement cascade is activated during cardiopulmonary bypass (CPB) and in trauma victims. In order to study whether plasma expanders may contribute to complement activation in these settings, fresh human serum was incubated with dextran 70 and polygeline. C3-activation products and the terminal complement complex (TCC) were quantified in enzyme immunoassays. At 37 degrees C, dextran caused immediate, dose-dependent C3 activation and TCC formation with decline later in the rate of TCC formation relative to serum-saline controls. High doses of polygeline caused slight activation after 15-30 min. The authors tested also the activation under conditions comparable to those found during clinical CPB. Activation induced by dextran and polygeline was increased by dilution of the serum. Furthermore, the plasma expanders counteracted the well-known inhibitory effects of heparin (4 IU/ml) and moderate hypothermia (30 degrees C) on complement activation. The authors conclude that dextran, and to a lesser extent polygeline, may contribute to complement activation during CPB and other clinical settings such as shock treatment.

Cardiopulmonary Bypass↗
PubMed1985

Three per cent dextran-60 as a plasma substitute in blood component therapy. I. An alternative in surgical blood loss replacement.

Microaggregate-poor erythrocyte concentrate with 3% dextran-60 as a plasma substitute was compared with microaggregate-poor whole blood for replacement of intra-operative and immediately postoperative blood loss. Sixty patients undergoing total hip arthroplasty randomly received either of these two forms of therapy. In accordance with the clinical routine of our orthopedic department, an infusion of 500 ml of 6% dextran-70 (Macrodex) was given as thrombo-prophylaxis in both groups. Use of 3% dextran-60 as a plasma substitute in blood component therapy for surgical hemorrhage of up to 50% of the calculated blood volume caused no increase in bleeding tendency or frequency of postoperative hematoma compared with whole blood replacement. Plasma protein levels were low immediately postoperatively in patients given the dextran, but from the 4th postoperative day onward there was no difference between the groups. Applied in clinical practice, this would be efficient in saving plasma for other urgent purposes.

Aged↗
PubMed1975

The effective oncotic pressure of dextran.

Measurement of plasma volume before and after the acute infusion of commercial dextran revealed that all brands tested were hyperoncotic by a factor of approximately 2. By mixing 6% dextran with 0.9% saline in 1:1 proportion a 3% dextran solution was obtained which was nearly isoncotic in our dogs. The most likely explanation for the discrepancy is that the 6% solution contains a high proportion of molecules of lower molecular weight resulting in a greater oncotic pressure than predicted on the basis of the average molecular weight. In addition, this leads to a rapid loss of this solute from the blood. Clinicians and researchers should be aware of the possibility that the dextran preparation they are using is not truly isoncotic.

Animals↗
PubMed1991

Effect of dextrans of various molecular weights on mesangial transport in ddY mice pretreated with sheep anti-type IV collagen serum.

The authors' previous report concluded that increased mesangial IgA deposition seen in ddY mice pretreated with mesangiotropic anti-type IV collagen serum might be due to a dysfunction of mesangial transport of macromolecules such as polymeric autologous IgA. In the present study we examined the effect of macromolecules upon mesangial transport in similarly treated ddY mice, using intravenously administered FITC-labeled dextrans of various molecular weights as tracers. The intensity of each resulting mesangial dextran deposit inspected directly by immunofluorescence was measured periodically and compared with the deposition of autologous mouse IgA examined using rhodamine-labeled rabbit anti-mouse IgA. High-molecular-weight dextran of 2,000 kDa showed prolonged mesangial deposition which paralleled the intensity and distribution of the autologous mouse IgA deposition. In contrast, medium- and low-molecular-weight dextrans of 500 and 150 kDa, respectively, disappeared earlier from the mesangium, unlike the autologous IgA deposition which persisted. Based on these results, it was concluded that the macromolecularity of certain substances and a transport dysfunction of the mesangium may both be major factors in prolonged mesangial deposition. These findings may provide some clues to help clarify the pathogenesis of human IgA nephritis.

Animals↗
PubMed1978

Beads of a dextran polymer for the local treatment of cutaneous ulcers.

A new polymer of dextran in the form of beads, 0.1 to 0.3 mm in diameter, was applied topically to 39 cutaneous ulcers of various causes. The material, which is powerfully hydrophilic, promptly absorbed serous and purulent exudate from the surfaces of the ulcers. This action decreased the bacterial load and prevented crust formation. Healthy granulation tissue then developed quickly in many ulcers and healing time seemed to be shorter in some cases. The exudate-absorbing capability of the beads of dextran was particularly beneficial in ulcers that had uneven surfaces, undercut margins, and sinus tracts. Complete healing was achieved in some of these cases that had previously resisted many kinds of treatment. The most important undesirable effect of the beads of dextran is their tendency to dehydrate the bases of ulcers too much, which slows or stops healing in some cases. This effect may be overcome by alternating applications of the material with hydrating forms of treatment or changing entirely to such treatment when applications of the beads has removed all exudate from the ulcers. No allergic, irritant, or toxic reaction from the dextran was encountered.

Aged↗
PubMed2006

A new synbiotic, Lactobacillus casei subsp. casei together with dextran, reduces murine and human allergic reaction.

We studied the development of atopic dermatitis-like skin lesions in NC/Nga mice and the allergic symptoms and blood patterns of healthy volunteers during the cedar (Cryptomeria japonica) pollen season in Japan following oral administration of a new synbiotic, Lactobacillus casei subsp. casei together with dextran. The combination of L. casei subsp. casei and dextran significantly decreased clinical skin severity scores and total immunoglobulin E levels in sera of NC/Nga mice that had developed picryl chloride-induced and Dermatophagoides pteronyssinus crude extract-swabbed atopic dermatitis-like skin lesions. During the most common Japanese cedar pollen season, synbiotic L. casei subsp. casei and dextran in humans led to no significant changes in total nasal and ocular symptom scores, in the levels of cedar pollen-specific immunoglobulin E, interferon-gamma and thymus and activation regulated chemokine or in the number of eosinophils in sera, whereas the placebo group showed a tendency for increased levels of cedar pollen-specific immunoglobulin E, thymus and activation regulated chemokine and number of eosinophils, and a decrease in interferon-gamma levels. Thus, the oral administration of synbiotic L. casei subsp. casei together with dextran appears to be an effective supplement for the prevention and treatment of allergic reactions.

Adult↗
PubMed1992

Priming effect of dextran sulphates on lipopolysaccharide-induced tumour necrosis factor production in mice.

Dextran sulphate (DS) 500 (M.W. 500,000) is commonly used as a reticuloendothelial (RE) blocker. We found that lipopolysaccharide (LPS)-induced tumour necrosis factor (TNF) production in sera was enhanced when mice were pretreated with DS500. When mice were pretreated with DS1000 (M.W. 1,000,000), TNF activity in sera was also significantly enhanced by the LPS injection in comparison with the saline-treated group, but not by the pretreatment with the low molecular weight of DS5 (M.W. 5,000), neutral dextran (Dex) 500, or positively-charged diethylaminoethyl dextran (DEAE-Dex) 500. The enhancement of LPS-induced TNF production occurred from 2 h after DS500 pretreatment. Pretreatment with DS500 or DS1000 significantly suppressed the carbon clearance from the blood in mice from 2 h after DS injection, but this suppression was not detected by the pretreatment with DS5, Dex500, or DEAE-Dex500. We suggest that negative-charge and high molecular weight are essential for dextran derivatives to enhance LPS-induced TNF production, and that the enhancing effect of DS is closely related to the suppression of the RE function.

Animals↗
PubMed1984

Vascular permeability in acute triethyltin-induced brain edema studied with FITC-dextrans, sodium fluorescein and horseradish peroxidase as tracers.

In golden hamsters, a study was made on the vascular permeability changes which might take place during the formation of triethyltin (TET)-induced brain edema. For this purpose, the animals received a single intravenous (i.v.) injection of TET sulphate (5-10 mg/kg b.wt) and groups of animals were studied 4 to 24 h thereafter. By the use of a new density gradient technique based on polyvinylcoated silica particles (1), it was shown that white matter edema was present already at 4 h after the TET injection. The edema then progressed during the following 20 h. Electron microscopy revealed that fluid accumulated in myelin vacuoles of the hamsters in the same way as has been described in other animal species. The macromolecular tracer, horseradish peroxidase mol.wt 40,000 injected i.v., did not leak out of the cerebral vessels during the period when edema developed. In order to find out if the formation of edema is associated with a vascular permeability increase to other and smaller markers, we used several fractions of FITC-dextrans varying from mol.wt 3,000 to 70,000 and determined their intracerebral localization with a histotechnical procedure. FITC-dextrans, mol.wt 70,000, did not leak out of the cerebral vessels in any of the TET intoxicated hamsters during the observation period of 24 h. The same was true for most animals given the other dextran fractions. However, FITC-dextrans, mol.wt 3,000-20,000 were present outside the vessels in the edematous optic nerves and corpus callosum in a few TET treated animals taken 16-24 h after the TET injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1977

Iron-poly (sorbitol-gluconic acid) complex and iron-dextran in the treatment of severe iron deficiency anaemia.

An investigation has been carried out to study the efficacy of iron-poly (sorbitol-gluconic acid) complex (Ferastral) in the treatment of iron deficiency anaemia. Ferastral was given by the intramuscular route every second or third day in a dose of 500 mg, divided in two injections. These were compared with the results of a group treated with iron-dextran given by Total Dose Infusion (TDI). A total of 38 patients were treated with either Ferastral or iron-dextran by TDI, respectively, given according to random allocation. The total dose of iron given in both groups was 1 500 mg of elemental iron. The parameters investigated were haematocrit and haemoglobin. Side-effects were also recorded. The results in the group treated with Ferastral where the mean initial haemoglobin value was 9.5 g/100 ml showed a mean haemoglobin increase to 13.2 g/100 ml after eight weeks. Initial haemoglobin values and haemoglobin increase for iron-dextran by TDI were quite similar. Three patients in the Ferastral group had transient discolouration at the site of injection and one patient in the iron-dextran TDI-group had a serious allergic reaction.

Anemia, Hypochromic↗
PubMed1978

Dextran-induced lowering of prekallikrein proactivator and prekallikrein in rat plasma.

The intravenous injection into rats of dextran (average MW 70,000) 10 mg/100 g caused marked hypotension after a delay of about 5 minutes. Blood samples collected by cardiac puncture at this time were tested for the amounts of prekallikrein activator (PKA) and kallikrein after acetone- and then kaolin activation of the plasminogen-free plasma. PKA was assayed by measuring the initial rate of release of benzoyl arginine esterase (BAEe) activity in a preparation of partially purified human prekallikrein, and kallikrein was assayed by measuring the BAEe esterase activity. Significant reductions of both parameters were registered, and the amount of high molecular weight kininogen (HMWK) present in the plasma was also reduced. Pretreatment of the rats with epsilon-aminocaproic acid intraperitoneally (200-300 mg/100 g) abolished the dextran-caused decreases in the plasma levels of the above mentioned factors, and reduced the fall in blood pressure. The addition of purified human HMWK to the plasma before the acetone activation procedure was started, increased the yield of PKA activity in the final enzyme preparation. When PKA was assayed after kaolin activation of plasma at 0 degrees using the method developed by Laake & Vennerød (1973a & b) for the determination of PKA (activated factor XII) in human plasma, no differences were registered between plasma from rats treated with dextran and plasma obtained from control rats. It is suggested that the low PKA activity of the acetone activated enzyme preparation from plasma of rats treated with dextran was due to the loss of HMWK or a fraction of HMWK.

Acetone↗
PubMed2003

The interleukin-1 beta-converting enzyme inhibitor pralnacasan reduces dextran sulfate sodium-induced murine colitis and T helper 1 T-cell activation.

The proinflammatory cytokines interleukin (IL)-1beta and IL-18 are supposed to play a crucial role in the pathogenesis of human inflammatory bowel disease. To exert biological activity, the precursors of both IL-1beta and IL-18 need to be cleaved by the interleukin-1beta-converting enzyme (ICE). IL-18 induces the synthesis of IFN-gamma in T cells and NK cells. In the present study, we investigated the effect of the specific ICE inhibitor pralnacasan in dextran sulfate sodium-induced murine colitis. Colitis was induced in BALB/c mice by 3.5% dextran sulfate sodium dissolved in drinking water for 10 days. Pralnacasan was administered either intraperitoneally or orally every day. To assess in vivo efficacy, a clinical disease activity score was evaluated daily. Colon length, expression of IL-18 in colonic tissue, expression of interferon-gamma (IFN-gamma) in paraaortal lymphocytes, and systemic production of IFN-gamma in splenocytes were analyzed post mortem. Intraperitoneally administered pralnacasan significantly reduced the clinical score compared with the dextran sulfate sodium control group from day 6 to day 10. Oral administration of pralnacasan also significantly reduced the clinical score at days 8 and 9. Administration of pralnacasan i.p. reduced the expression of intracolonic IL-18 significantly. Furthermore, pralnacasan reduced the number of IFN-gamma-positive lymphocytes in paraaortal lymph nodes. IFN-gamma synthesis in stimulated splenocytes was significantly suppressed in all pralnacasan-treated groups. No side effects of pralnacasan were observed. In conclusion, pralnacasan is effective in the prevention of dextran sulfate sodium-induced colitis. This effect is probably mediated by suppression of the proinflammatory cytokines IL-18, IL-1beta, and IFN-gamma.

Animals↗
PubMed1977

Distribution of dextransucrase in Streptococcus mutans and observations on the effect of soluble dextran on dextransucrase activities.

Total and insoluble dextransucrase activities were measured in cell-associated and supernatant fractions of Streptococcus mutans GS-5 grown in several media. Although the amount of cell-associated and supernatant activity varied greatly as a function of medium, the total activity appeared constant. The distribution of dextransucrase could be altered without changing the total dextransucrase activity. This indicates that the distribution of the enzyme can be regulated independently of its synthesis. Strain GS-5 had significant cell-associated activity in media devoid of sucrose. In all cases, the ratio of insoluble to total dextransucrase activity was higher in the cell-associated fractions than in the cell-free supernatants. It is also demonstrated that exogenous soluble dextran caused a decrease in insoluble dextransucrase activity and an increase in soluble dextransucrase activity in both the cell-associated fraction and the culture supernatant. The stimulation of soluble dextran-synthesizing activity was not due to de novo synthesis. The inhibition of insoluble dextran-synthesizing activity is shown to be noncompetitive. These results support a physical rather than metabolic mechanism for the effect of soluble dextran on dextransucrase activities.

Chloramphenicol↗
PubMed1995

Local and systemic antibody responses to dextran-cholera toxin B subunit conjugates.

This study was designed to test local and systemic immunity following mucosal immunization with a polysaccharide-protein conjugate. After preparing and characterizing dextran-cholera toxin B subunit (CTB) conjugates, we studied their immunogenicity in mice following systemic or mucosal immunizations. Dextran was chosen as a model polysaccharide antigen and conjugated via adipic acid dihydrazide and N-succinimidyl-3-(2-pyridyldithio)propionate to CTB. Mice were immunized either subcutaneously, intranasally, or perorally three times, and cholera toxin was used as an adjuvant for the mucosal immunizations. Three conjugates with different molecular weights for dextran (40,000 and 76,000) or varying dextran/CTB molar ratios were tested. Peroral immunizations with all conjugates evoked local immunoglobulin A (IgA) antibody responses against dextran in the small intestine, and intranasal immunizations did the same in the lung. Intranasal immunizations also elicited serum antibody titers that were significantly higher than or equal to those after subcutaneous immunizations. Intranasal immunizations evoked serum IgG antidextran titers which were dependent on the dextran/CTB molar ratio and inversely related to the local IgA response, which was not the case for subcutaneous immunizations. This is the first study of local and systemic immunity following mucosal immunization with a polysaccharide-protein conjugate. The results show that it is possible to evoke a local as well as a systemic antibody response against a polysaccharide by conjugating it to CTB and using an appropriate route of immunization.

Administration, Intranasal↗
PubMed2000

Pathogenesis of infection by clinical and environmental strains of Vibrio vulnificus in iron-dextran-treated mice.

Vibrio vulnificus is an opportunistic pathogen that contaminates oysters harvested from the Gulf of Mexico. In humans with compromising conditions, especially excess levels of iron in plasma and tissues, consumption of contaminated seafood or exposure of wounds to contaminated water can lead to systemic infection and disfiguring skin infection with extremely high mortality. V. vulnificus-associated diseases are noted for the rapid replication of the bacteria in host tissues, with extensive tissue damage. In this study we examined the virulence attributes of three virulent clinical strains and three attenuated oyster or seawater isolates in mouse models of systemic disease. All six V. vulnificus strains caused identical skin lesions in subcutaneously (s.c.) inoculated iron dextran-treated mice in terms of numbers of recovered CFU and histopathology; however, the inocula required for identical frequency and magnitude of infection were at least 350-fold higher for the environmental strains. At lethal doses, all strains caused s. c. skin lesions with extensive edema, necrosis of proximate host cells, vasodilation, and as many as 10(8) CFU/g, especially in perivascular regions. These data suggest that the differences between these clinical and environmental strains may be related to growth in the host or susceptibility to host defenses. In non-iron dextran-treated mice, strains required 10(5)-fold-higher inocula to cause an identical disease process as with iron dextran treatment. These results demonstrate that s.c. inoculation of iron dextran-treated mice is a useful model for studying systemic disease caused by V. vulnificus.

Animals↗
PubMed1977

Ultrastructural surface changes associated with dextran synthesis by Leuconostoc mesenteroides.

When Leuconostoc mesenteroides NCDO 1875 was grown in MRS broth and fixed for electron microscopy in the presence of ruthenium red, the cell wall appeared as a triple-layered structure similar to other, gram-positive bacteria. When such logarithmic-phase cultures were exposed to sucrose, the appearance and growth of a uniform layer of electron-dense material was evident on the surface of the cell wall. After 2 h in the presence of sucrose, the formation of this surface coat (110 to 130 nm thick) was complete. For 85 to 90% of the cells, continued exposure to sucrose did not produce any further change in their appearance, but the rest of the population began to accumulate insoluble capsular dextran at the surface of their coat material. Within 18 h, these cells had produced a large capsule (maximum diameter, 6 micrometer) composed mainly of an extensive reticulum of fine filaments. Periodate-reactive carbohydrate was localized cytochemically in the capsular dextran and in the surface coat of all cells. It is suggested that the surface coat of sucrose-grown cells represents a cell-bound dextran-dextransucrase complex and that the acapsulate cells produce the relatively soluble S dextran reported by previous workers.

Cell Wall↗
PubMed1967

Effect of diethylaminoethyl dextran on the growth of Mycoplasma in agar.

The growth of certain strains of Mycoplasma is inhibited by substances present in commercial agar preparations. The addition of diethylaminoethyl (DEAE) dextran (10 mg per 100 ml) to agar media appears to enhance the growth of some strains. Of eight strains initially tested, the presence of DEAE dextran grossly enhanced the growth of three strains. One strain appeared not to be affected, and a clearly enhancing effect was not evident with four strains. Quantitative studies revealed that growth enhancement varied from 10 colony-forming units (CFU) for M. hominis type II (strain Campo) to 10(3.3) CFU for M. pulmonis (strain 880). The growth-enhancing effect is probably due to the ability of DEAE dextran to bind the sulfated polysaccharide moieties in agar and not to the DEAE dextran, per se.

Agar↗
PubMed1972

Control of interferon synthesis: effect of diethylaminoethyl-dextran on induction by polyinosinic-polycytidylic acid.

Interferon production in cultures of rabbit kidney cells (RKC) stimulated with 10 to 250 mug of polyinosinic-polycytidylic acid (poly I.poly C) per ml peaked at 3 to 4 hr after the exposure of cells to inducer and rapidly declined thereafter. On the other hand, RKC stimulated with poly I.poly C (10 or 2 mug/ml) in the presence of diethylaminoethyl (DEAE)-dextran (100 or 20 mug/ml, respectively) produced a protracted interferon response, with the release of interferon continuing for over 24 hr. The kinetics of interferon production in RKC stimulated with lower concentrations of the mixture of poly I.poly C and DEAE-dextran were similar to the response produced by poly I.poly C alone (10 to 250 mug/ml). Only the responses that terminated early were paradoxically enhanced by treatment with low doses of actinomycin D or with cycloheximide. Cells stimulated with 50 mug of poly I.poly C/ml showed hyporesponsiveness to a second interferon induction with poly I.poly C when restimulated 7 hr after primary induction. This hyporesponsiveness could be overcome by restimulating with higher concentrations of the poly I.poly C-DEAE-dextran complex. The results are compatible with the hypothesis that the early termination of interferon production and hyporesponsiveness to repeated induction with poly I.poly C are due to a cellular repressor exerting negative control on interferon synthesis, and that the increased cellular uptake of poly I.poly C in the presence of DEAE-dextran may effectively neutralize the repressor. These results also suggested that the often observed different kinetics and the varied effects of inhibitors of ribonucleic acid or protein synthesis on interferon responses in various cells and in cells stimulated with different inducers (such as with viruses as compared with polynucleotides) need not imply the existence of fundamentally different mechanisms of interferon production.

Animals↗
PubMed2005

Microbial dextran-hydrolyzing enzymes: fundamentals and applications.

Dextran is a chemically and physically complex polymer, breakdown of which is carried out by a variety of endo- and exodextranases. Enzymes in many groups can be classified as dextranases according to function: such enzymes include dextranhydrolases, glucodextranases, exoisomaltohydrolases, exoisomaltotriohydrases, and branched-dextran exo-1,2-alpha-glucosidases. Cycloisomalto-oligosaccharide glucanotransferase does not formally belong to the dextranases even though its side reaction produces hydrolyzed dextrans. A new classification system for glycosylhydrolases and glycosyltransferases, which is based on amino acid sequence similarities, divides the dextranases into five families. However, this classification is still incomplete since sequence information is missing for many of the enzymes that have been biochemically characterized as dextranases. Dextran-degrading enzymes have been isolated from a wide range of microorganisms. The major characteristics of these enzymes, the methods for analyzing their activities and biological roles, analysis of primary sequence data, and three-dimensional structures of dextranases have been dealt with in this review. Dextranases are promising for future use in various scientific and biotechnological applications.

Bacteria↗