[Modulatory effect of isoniazid and rifampicin in vitro on cytokine secretion in pulmonary tuberculosis].

The effects of isoniazid and rifampicin on the peripheral mononuclear production of IL-2, IL-12, IL-10, IFN-gamma, and TGF-beta were evaluated in patients with infiltrative pulmonary tuberculosis. Irrespective of the susceptibility of the causative agent to the essential antituberculous drugs, rifampicin was ascertained to initiate increased IL-2 secretion and to reduce the generation of IL-12, IFN-gamma and TGF-beta. Isoniazid suppressed the mononuclear leukocytic production of IFN-gamma in drug-sensitive pulmonary tuberculosis, and conversely, stimulated it in the drug-resistant type. Rifampicin showed a more significant negative effect on mononuclear cytokine-producing activity. In drug-resistant pulmonary tuberculosis, the imbalance of spontaneous, protein- and drug-induced mononuclear secretion of cytokines was established to be more pronounced than in drug-sensitive tuberculosis.

[The molecular-genetic aspects of tubercular infection forecasting and immunotherapy].

In article is presented, the analysis of the data of the literature and own researches, concerning molecular-genetic mechanisms of antimycobacterial immunity infringements. The role of the factors defining features of a current and an outcome of a tubercular infection, namely of immunity system condition, feature of infecting microbic Mycobacterium tuberculosis strain biological properties (a genotype, a spectrum of drag sensitivity/resistance), influence of combined antitubercular chemotherapy is disc issed. The opinion is expressed that the given factors are necessary for taking into consideration for working out methodology the personalised preventive maintenance and correction of immunity infringements during pulmonary tuberculosis.

[Evaluation of the effects of antituberculous drugs on the cytochemical status of lymphocytes in vitro].

The effects of basic drugs of chemotherapy for tuberclosis, such as isoniazid and rifampicin, on the activity of the most important mitochondrial enzymes of lymphocytic energy metabolism were studied in patients with infiltrative tuberculosis and healthy donors. The authors detected the significantly inhibited activity of succinate dehydrogenase and the redistribution of lymphocytic populations with the increased proportion of cells with the low and high activities of the enzyme. The more significant negative effect on the lymphocytes of patients with tuberculosis was observed when rifampicin was administered. In patients with pulmonary tuberculosis, the suppressed enzymatic activity of peripheral blood lymphocytes was shown to be more pronounced when the cells were incubated with rifampicin and isoniazid for 2 hours than for 1 hour.

[Role of cytokines in the modulation of lymphocytic subpopulational composition in patients with pulmonary tuberculosis].

The parameters of the lymphocytic CD-population composition and the production of cytokines in the cell cultures of peripheral blood mononuclear cells were studied in patients with infiltrative pulmonary tuberculosis. A marked reduction in the relative and absolute count of CD3+ and CD4+ lymphocytes and an increase in the level of CD8- and CD16-positive cells were established in both drug-sensitive and drug-resistant types of the disease. A significant increase in the production of IL-12 and a reduction in the spontaneous elaboration of interferon-gamma were observed in all the examinees. Addition of lipid and protein myobacterial antigens (Beijing strains) caused a notable decrease in the generation of the study cytokines as compared with the respective parameters in healthy donors and their basal secretion irrespective of the type of a tuberculous process.

[Immune pathology in pulmonary tuberculosis].

The data of modem literature and the results of original investigations on mechanisms of immunopathological alterations in tuberculosis infection are presented. The role of cellular and humoral parts of immunity in pathogenesis of pulmonary tuberculosis is discussed and cytokine-mediated mechanisms of disorders in a specific immune response are analysed.