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Z Zidek

Publications and source records attributed to Z Zidek.

11 recordsLinked to original sources
PubMed1999

Interleukin-10 in combination with interferon-gamma and tumor necrosis factor-alpha enhances in vitro production of nitric oxide by murine resident paritoneal macrophage.

Resident peritoneal macrophages obtained from CBA/J mice were cultured in the presence of recombinant interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), and interleukin-10 (IL-10). IFN-gamma-stimulated nitric oxide (NO) formation, IL-10 substantially enhanced the production of NO generated by IFN-gamma + TNF-alpha, irrespective of the timing and dosing of any of the three cytokines. Increased levels of iNOS mRNA after the triple combination of IFN-gamma + TNF-alpha + IL-10 versus IFN-gamma + TNF-alpha suggest that the NO-enhancing effect is mediated, at the least partially, at the transcriptional level. Collectively, the present data support the view that IL-10 is not a general macrophage deactivating factor or a suppressor of gene expression.

Animals↗
PubMed1999

Adenosine - cyclic AMP pathways and cytokine expression.

Adenosine and cAMP are potent modulators of immune-triggered cytokine production. Their effects overlap with regard to the inhibition of the pro-inflammatory cytokines TNF-alpha, IFN-gamma, IL-12, and the stimulation of production of the major anti-inflammatory cytokine IL-10. They may tentatively be considered to be upregulators of the production of Th2 cytokines (IL-10, IL-6), but downregulators of the production of Th1 cytokines (IL-2 and IFN-gamma). Cytokines produced in common by Th0, Th1 and Th2 cells are affected as well, although the low quantity and heterogeneity of the contemporary experimental data do not allow unambiguous conclusions to be drawn. Nevertheless, IL-3, IL-4, MIP-1alpha/beta and GM-CSF have usually been found to be inhibited, IL-5 stimulated, while IL-1 remains largely unaffected by adenosine or cAMP. These effects, and in particular the inhibition of TNF-alpha and stimulation of IL-10 expression, might be of therapeutic value in a variety of pathophysiological conditions.

Adenosine↗
PubMed1998

IFN-gamma-induced TNF-alpha is a prerequisite for in vitro production of nitric oxide generated in murine peritoneal macrophages by IFN-gamma.

The effect of IFN-gamma to stimulate formation of nitric oxide (NO) by normal murine peritoneal macrophages (M phi) has been found to be completely dependent on the ability of IFN-gamma to activate secretion of TNF-alpha. The NO-stimulatory effect of IFN-gamma was abolished by anti-TNF-alpha antibodies, the inhibitory intervention of which could be fully reversed by exogenously supplied TNF-alpha. Accordingly, the failure of M phi from C3H/HeJ mice to secrete TNF-alpha upon stimulation with IFN-gamma was associated with their complete incapability to generate NO, unless they were simultaneously treated with IFN-gamma + TNF-alpha. Collectively, the data document that similar to the NO up-regulatory action of other cytokines, the effect of IFN-gamma is not independent, but depends on a synergistic cooperation with the self-produced TNF-alpha. The findings thus indicate that a widespread opinion claiming that IFN-gamma per se is able to stimulate biosynthesis of NO needs revision.

Animals↗
PubMed1998

Stimulation of macrophages by Bacillus firmus: production of nitric oxide and cytokines.

Immunostimulatory properties of gram-positive Bacillus firmus were investigated under in vitro conditions using murine peritoneal macrophages. B. firmus stimulated in a concentration and time dependent manner the secretion of tumour necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10), but it had no influence upon interferon-gamma (IFN-gamma) and interleukin-2 (IL-2) production. It also substantially augmented production of nitric oxide (NO) induced by exogenous IFN-gamma. Inhibitory experiments using neutralizing antibodies against TNF-alpha and/or IL-10 have demonstrated that these cytokines are responsible for triggering the underlying mechanism(s) leading to enhanced NO production. The cytokine-stimulatory and NO-costimulatory properties could participate in the antiinfectious and anticancer effects of B. firmus, detected previously in the in vivo experiments.

Animals↗
PubMed1998

Erratic behavior of nitric oxide within the immune system: illustrative review of conflicting data and their immunopharmacological aspects.

The literature data assembled in this article document the variation of immunobiological effects of nitric oxide (NO). A number of factors are obviously responsible for the diversity, ranging from inactivity, alleviation, but not rarely to exacerbation of certain pathogenetic processes. A better understanding of NO interactions with the immune system can only be reached if more complex experimental designs to study the effects of reactive nitrogen species are adopted in the future. They should integrate major participating variables and take into account pharmacodynamic/kinetic aspects of NO production in triggering the ultimate effects. If manipulation of NO in the organism by means of recently developed NO inhibitors and NO donors is to become a rational tool of immunopharmacological strategies, detailed knowledge of their pharmacologies and toxicologies is urgently needed in order to differentiate between the effects of NO and other side effects. Hopefully, this approach could improve the predictability of the clinical outcomes of NO manipulation.

Animals↗
PubMed1996

Effect of adamantylamide dipeptide on reinfection resistance after primary infection eradication in experimental Schistosomiasis mansoni.

The immunomodulatory effect of adamantylamide dipeptide (AdDP) was tested in Schistosoma mansoni-infected challenged mice and infected praziquantel-treated (2 x 500 mg/kg) challenged animals. In AdDP-treated mice, the drug was given 58 days post infection of mice with 120 S. mansoni cercariae, challenged with 240 cercariae one day after treatment, while in praziquantel-treated mice, the drug was given 44 days post infection, two weeks post treatment (58 days post infection) they were given AdDP in the same dose and one day later challenged with the same cercarial load. AdDP increased the resistance against reinfection (90.3% vs. 83.5% in infected challenged control). The significant increase in resistance against reinfection was accompanied by significant increase in the percentage of lymphocytes forming EAC rosettes. Mice cured of their primary infection by praziquantel showed a significant reduction in percent resistance, hepatic granuloma size and intragranulomal Thy+ 1,2 and Lyt+ 1 T cells. In mice treated with both praziquantel and AdDP, resistance to reinfection was significantly higher than in mice treated with praziquantel only (89.29% vs. 62.13%) reaching a level comparable to that recorded in infected-challenged controls. Meanwhile granuloma size was not significantly different from that in the infected-challenged controls with a significant rise in Lyt+ 1 T cells. Data may suggest a role for granuloma as a mechanical obstacle and/or as a T cell-mediated reaction in maintenance of resistance to reinfection. A role for B lymphocytes should be considered as the rise of percent resistance to reinfection in mice treated with AdDP alone was accompanied by a significant increase in the percentage of B lymphocytes forming EAC rosettes. Moreover, findings may suggest the use of AdDP together with specific chemotherapy in endemic areas where reinfection and repeated treatment with its consequences are of common occurrence.

Adjuvants, Immunologic↗
PubMed1988

[Participation of the dopaminergic system in the immune response-stimulating effect of muramyl dipeptide].

It has been shown that administration of muramyl dipeptide (MDP) in a dose of 1 mg/kg simultaneously with SRBC (5 x 10(6) immunization resulted in a considerable increase of immune response. Stimulation of the immune response is prevented by preliminary blockade of dopamine receptors with haloperidol, that testifies to the activation of the dopaminergic system by certain MDP dosages.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1987

No evidence for an interaction of the bacterial immunomodulator trehalose dimycolate (TDM) with liver drug-metabolizing system in mice.

Trehalose dimycolate (TDM), an immunomodulatory glycolipid component of Mycobacteria, was tested from the point of view of possible effects on drug metabolism. TDM was given intraperitoneally as a single 0.1 mg dose to mice. Basic parameters of the liver mixed-function oxidase system were assayed 1 or 7 days later. No significant changes were found in contents of cytochromes P-450 and b5, as well as in specific activities of microsomal enzymes--aniline hydroxylase, ethylmorphine demethylase, and glucuronide transferase. Similarly, liver microsomal protein concentration and activities of serum aspartate and alanine transaminases remained unchanged. The susceptibility of microsomal membranes to lipid peroxidation was significantly decreased 7 days after TDM administration. TDM may thus be presumed not to influence range and magnitude of effects of concurrently administered drugs.

Animals↗
PubMed1979

Estrogen-dependent differences in the acetylation of sulfadimidine in the rat.

The influence of sex hormones on the acetylation of sulfadimidine was investigated in male and female rats, both intact and castrated. Sulfadimidine was administered intravenously in the dose of 40 mg/kg body weight, and unchanged and acetylated sulfadimidine (Ac-S) were then determined in urine and blood. It was found that the percentage of Ac-S was significantly higher in the urine of females than males. The concentration of sulfadimidine in blood was also higher in females than in males. While estrogenization raised the percentage of Ac-S in the urine of males and the concentration of unchanged sulfadimidine in blood, treatment with an androgen had no significant effect in females. The long-lasting stimulatory influence of estrogen in males and a normal percentage of Ac-S in gonadectomized females suggest an indirect action of estrogen. Possible mechanisms are discussed.

Acetylation↗