[Cytokine production during the development and correction of an immunodeficiency in experimental tuberculosis]. / Produktsiia nekotorykh tsitokinov v khode razvitiia i korrektsii immunodefitsita pri eksperimental'nom tuberkuleze.

The authors investigated spontaneous and induced secretion of cytokins at different stages of generalized tuberculosis. In the development of infection there were inhibited IL-2 synthesis in response to ConA, emerging activity of PNO-alpha in response to the inductors in blood serum and culture of peritoneal macrophages, enhanced secretion of IL-6. Complete immunodeficiency was associated with cessation of IL-2 synthesis by splenocytes, elevated production of IL-6 by peritoneal macrophages, low concentrations of PNO-alpha in the serum and peritoneal macrophage cultures. In the treatment of M. bovis-infected mice with antibacterial drugs alone IL-6 secretion by peritoneal macrophages and PNO-alpha activity in the serum were increased. Immunocorrection resulted in marked activation of IL-2 production by splenocytes in response to ConA as well as enhanced synthesis of IL-6 in unstimulated cultures of peritoneal macrophages.

[Coxiella burnetii antigens--inducers of tumor necrosis factor and interleukin-1]. / Antigeny Coxiella burnetii--induktory faktora nekroza opukholi i interleikina-1.

The cultivation of mouse peritoneal macrophages in the presence of antigenic preparations obtained from C.burnetii was accompanied by the appearance of phagocytes and considerable amounts of tumor necrosis factor and interleukin 1 in the culture medium. The production of cytokines depended on the doses of preparations used as inducers. The special treatment of C.burnetii antigen, selectively removing its phospholipid components, led to a sharp drop in its capacity for stimulating the production of cytokines.

[The role of tumor necrosis factor and interleukin-1 in forming resistance in experimental Q fever]. / Rol' faktora nekroza opukholi i interleikina-1 v formirovanii rezistentnosti pri éksperimental'noi Ku-likhorade.

Preliminary injections of human recombinant tumor necrosis factor (TNF-alpha) and interleukin 1 (IL-1 beta) increases the resistance of guinea pigs to Coxiella burnetii. The increase of this resistance depends on the dose of cytokines and the time of their inoculation.

[The induction of tumor necrosis factor and interleukin-1 under exposure to the glycopolymers isolated from Pseudomonas solanacearum and Clavibacter michiganense]. / Issledovanie induktsii faktora nekroza opukholi i interleikina-1 pod vozdeistviem glikopolimerov, vydelennykh iz Pseudomonas solanacearum i Clavibacter michiganense.

Lipopolysaccharide of Pseudomonas solanacearum and acid polysaccharides of Clavibacter michiganense are effective inductors of formation of the factor of tumour necrosis (TNF) and interleukin-1 (IL-1) by peritoneal macrophages of mice and their activity exceeds that of lipopolysaccharide Escherichia coli 055:B5 ("Sigma"). O-specific polysaccharide and lipid A are responsible for the capacity of liposaccharide molecule of P. solanacearum to induce TNF and IL-1.

[Mechanism of the anti-tumoral effect of the blastolysin fraction isolated from Lactobacillus bulgaricus]. / K mekhanizmu protivoopukholevogo deistviia fraktsii blastolizina, vydelennoi iz Lactobacillus bulgaricus.

A blastolysin fraction, isolated from lysosyme lysates of Lactobacillus Bulgaricus strain 51 by gel chromatography, was shown to markedly inhibit the growth of sarcoma S-180. A single administration of the agent was followed by an insignificant decrease in tumor growth rate, while repeated treatment induced a complete regression of tumor in 15% of animals and resulted in a prolonged suppression of tumor growth in the others. Cells isolated from metastases which developed after the withdrawal of the drug retained susceptibility to fraction 2 of blastolysin. The latter fraction showed a similar pattern of inhibition of the growth of Ehrlich ascites tumor but did not affect hemocytoblastosis in mice LA. Histologically, fraction 2 produced tumor cell necrosis which commenced at 24 hours posttreatment. Such signs of hypercorticoidism as lysis of lymphocytes in the cortical layer of the thymus, depletion of T-dependent zones of spleen and lymph nodes and adrenal cortical hyperplasia were registered. Macrophage level in tumor was not increased. A 7-fold rise in murine serum corticosterone level at 1 hour posttreatment was established by the method of competitive protein binding.