摘要:

AbstractThe anti-HIV activities of two new polyanionic polymers (AM 242 and AM 612) were investigated in cell culture-based and biochemical antiviral assays. These compounds inhibited the reverse transcriptases from HIV-1 and HIV-2, using enzyme purified from virions and either a ribosomal RNA or gapped duplex DNA as the template. With the ribosomal RNA template, AM 242 and AM 612 had ID50values of 1.1 and 0.10μg/ml against the HIV-1 reverse transcriptase.In vitrocell based assays determined that both compounds significantly inhibited both the cytopathic effects associated with HIV-1 infection and the replication of virus in infected cells. AM 242 had an IC50of approximately 1.0μg/ml, while that of AM 612 was 0.19μg/ml. These two active polyanionic polymers were effective in inhibiting the growth of a panel of HIV-1 isolates and were also active against HIV-2. Although the compounds were toxic at high concentration, they had antiviral activity over a wide range of nontoxic concentrations, yielding a high selectivity index. AM 612 was 100% protective for CEM cells from 320 ng/ml to 1μg/m1 Both compounds caused a significant increase in cellular proliferation as determined by the concentration-dependent increase in incorporation of radioactive precursors into cellular macromolecules.

ISSN:0892-3973    

DOI:10.3109/08923979209009229

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

AbstractThe effect of several divalent metal cations (Co, Cu, Zn, Hg and Pb) on the proliferative response of B9 hybridoma cells to IL-6 has been investigated. At concentrations which are not cytotoxic all the metals inhibited proliferation. The inhibition by Cd and Pb was dependent on both time of addition of the metal and IL-6 concentration. Cd (10μM) and Pb (50μM) added at the same time as IL-6 were inhibitory but added 24h later had no effect. Increasing the concentration of IL-6 overcame the inhibitory effect of Cd (10μM) and Pb (50μM). Inhibition caused by the other metals was independent of either time of addition or IL-6 concentration. IL-6 did not stimulate an increased intracellular concentration of metallothionein suggesting that the protective effect of IL-6 is not mediated via induction of metallothionein. The results suggest that there are at least two distinct metal sensitive events In B9 proliferation, i) IL-6 reversible inhibition by Cd and Pb ii) IL-6 Independent inhibition by Co, Cu and Hg.

ISSN:0892-3973    

DOI:10.3109/08923979209009230

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

AbstractExperiments were performed to analyze the possible effect of the immunomodulating agent Pidotimod (3-L-pyroglutamyl-L-thiazolidine-4-carboxylic acid) on mouse Natural Killer (NK) cell activity and glucocorticoid hormone(GCH)-induced thymocyte apoptosis. The results indicate thatin vivotreatment with Pidotimod (200 mg/Kg ip for 5 days) causes a significant increase in NK activity andin vitrotreatment produces a significant reduction of dexamethasone-induced thymocyte apoptosis. This inhibition appears to be dose-dependent and is also evident against TPA or Ca++ionophore-induced apoptosis.

ISSN:0892-3973    

DOI:10.3109/08923979209009231

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

ISSN:0892-3973    

DOI:10.3109/08923979209009232

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

AbstractIn this study we have investigated the role of PGE2 in the activation of human T lymphocytes by PWM. A preincubation of these cells with molar concentrations of the prostaglandin ranging from 10-9M to 10-4M is able to reduce the expression of IL-2R and CD71 on T lymphocyte membrane during the first days of culture, while the DR molecule which is expressed later in the same experimental conditions is not affected by the treatment of T lymphocytes with PGE2. The PGE2-induced inhibition of IL-2R and CD71 well correlates with the reduction of3H-thymidine incorporation by T cells, indicating that a preincubation of T lymphocytes with PGE2 profoundly affects the proliferative apparatus of these cells when they are stimulated by PWM.

ISSN:0892-3973    

DOI:10.3109/08923979209009233

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

AbstractEvaluation was carried out on the action of different antibiotics on the release of cytokines. Experiments were donein vitroon monocytes and on human lymphocytes. Results show that the majority of the antibiotics tested are able to induce the release of one or more cytokines from their respective producing cells. Among theβ-lactams the most active were the cephalosporins (cephalexin, cefamandol, ceftazidin, and a sulbactam-ampxcillin combination) in inducing the release of TNF, IL-1αand IL-6 from monocytes, and releasing IL-4 and IFN-τfrom lymphocytes. The sulbactam-ampicillin combination and cefamandole were extremely active in the production of IFN-τ. Among the lincosamides, clindamycine notably stimulated the release of TNF and IL-6, while lincomycine induced a notable increment of IL-4 from monocytes. Teicoplanin is a very strong inducer of TNF, IL-1αand IL-6.

ISSN:0892-3973    

DOI:10.3109/08923979209009234

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

AbstractThe modulatory effects of serotonin on T-cell activity were investigated. T-cell blastogenesis of normal spleen cells was slightly stimulated by the addition of low doses (1 and 10 ng/ml) of the inducer of serotonin release, fenfluramine. In contrast to the stimulatory effects of low doses of fenfluramine, high doses of fenfluramine (1 and 10 ug/ml) or of exogenously added serotonin (≥0.1 ug/ml) inhibited T-cell activation. Both the stimulation by low dose fenfluramine and the inhibition by high dose fenfluramine were accentuated by pretreating mice with tryptophan to heighten intracellular stores of serotonin and then inducing serotonin release. Pretreatment of mice with the serotonin inhibitor p-cholorphenylalanine (PCPA) abolished the fenfluramine inhibition of T-cell activation indicating that the fenfluramine inhibitory effect was mediated via endogenous spleen cell-derived serotonin. However, the PCPA treatment diminished T-cell activation. These results suggest that endogenous serotonin causes a biphasic dose-response effect on T-cell activity with serotonin being required for optimal T-cell function, low doses being immune stimulatory and higher doses being suppressive.Con-A, concanavain A5-HT, 5-hydroxytryptamineLAK, lymphokine-activated killerNK, natural killerPCPA, p-cholorphenylalaninePHA, phytohemagglutinin

ISSN:0892-3973    

DOI:10.3109/08923979209009235

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

AbstractFourteen cephalosporins, 11 penicillins and 1 monobactam were evaluated for theirin vitromodulation of murine neutrophil cytokinesis. As a result, theβ-lactam antibiotics were placed into 6 groups based on their effect on random (R) and FMLP-directed (D) migration [Group 1 (no effect) : cephalosporin C; Group 2 (R→D↓): cloxacillin, cefotaxime, ceftazadime, cefuroxime, cephalothin, cephapirin, cephadine, nafcillin, piperacillin, ticarcillin, ampicillin, oxacillin, aztreonam; Group 3 (R↑D→): cephaloridine; Group 4 (R↑D↑): cefsulodin; Group 5 (R↑D↓): cefoperazone, cefoxitin, ceftriaxone, 6-amino-penicillanic acid; Group 6 (R↓D↓): cefadroxil, cefazolin, penicillin G, methicillin]. Trypan blue exclusion studies showed that inhibition of R and D by Group 6β-lactam antibiotics is not due to overt cytotoxicity.β-lactam antibiotics inhibiting D also increased neutrophil adherence to plastic at a concentration of 1000μM. Finally, the [Ca++] inhibitor chlorpromazine significantly abrogatesβ-lactam- and FMLP-directed migration at a test concentration of 1μM.

ISSN:0892-3973    

DOI:10.3109/08923979209009236

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

AbstractThe effect of zinc treatment on immune function and resistance against infection and tumor challenge was studied in mice. Swiss albino mice were treated with zinc acetate (3 mg/kg body weight) in one or two intraperitoneal injections. Various immune function assays were performed in treated animals. Zinc treatment to normal animals caused potentiation of T-lymphocyte and macrophage functions. Zinc treatment was also found to increase host resistance against Candida albicans and Semliki Forest virus infections. Increased resistance against endotoxin shock and Ehrlich's ascites tumor challenge was also observed in zinc treated animals. It can be stated from this study that zinc treatment potentiates the cell mediated immunity and host resistance against infection and tumor challenge.

ISSN:0892-3973    

DOI:10.3109/08923979209009237

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

AbstractThe effect of 2-carboxyethylgermanium sesquioxide (Ge-132) on the generation of splenic suppressor macrophages (S-MØ) in C3H/He mice (H-2k) immunized with allogeneic spleen cells from C57B1/6 mice (H-2b) was investigated. We have previously demonstrated that S-MØexpressing I-J antigen, which appeared during alloimmunization, inhibited cytotoxic T lymphocyte (CTL) generation in the MLR and the elimination of these S-MØbefore subjection to the MLR resulted in more effective generation of CTL. The CTL activity, which was determined in vivo by the Winn's test, was markedly enhanced when immunized mice received a 100 mg/kg dose of Ge-132. The compound was found to be the most efficacious when injected simultaneously with the immunization. The activity of allospecific CTL co-cultured with MØfractions obtained from immunized mice in a 4-h51Cr-release assay was shown to be 31% lysis of the target cells as compared with 90% lysis of the target cells in effector cells co-cultured with normal MØfractions. In contrast, effector cells co-cultured with MØfractions from Ge-132-treated immunized mice lysed 95% of the target cells. Analysis of the level of I-J antigen expression on macrophages (MØ) obtained from mice 7 days after immunization revealed a>2.5-fold increase, whereas I-A antigen expression remained constant when compared with splenic MØfrom naive mice. In contrast, the opposite effect on I-J and I-A antigen expression was observed in splenic MØfrom alloimmunized mice treated with Ge-132. These results suggest that Ge-132 could regulate CTL generation in alloimmunized mice by preventing the generation of I-J+S-MØ.Ge-132: 2-carboxyethylgermanium sesquioxide

ISSN:0892-3973    

DOI:10.3109/08923979209009238

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor