[Apoptosis of host cells regulation by Chlamydia].

In a study on the impact of chlamydial infection on host cell apoptosis, C. trachomatis were shown to protect host cell against staurosporin-induced apoptosis only at the middle stage of infection development (at 20 hours post infection), C. pneumoniae--at different stages of its growth cycle (from 2 to 7 day post infection). We found, that C. trachomatis elementary bodies fail to inhibit staurosporin-induced apoptotic stimuli. The clear antiapoptotic effect of cell lysate filtrate, infected with C. trachomatis, was demonstrated by cytometric analysis and luminescent microscopy. Our findings make it possible to use biochemical approach to identification of chlamydial antiapoptotic factors in future. Investigations directed at chlamydial antiapoptotic activities may aim to create the therapies of chronic chlamydial infection.

[The apoptosis-supressing activity of clamydia].

The paper covers data from literature, concerning the influence of bacteria upon apoptosis program of host's cells. The mechanisms of apoptosis induction and suppression, developed by bacteria and directed towards the maintenance of conditions favorable to the infection, are quite varied. These mechanisms are realized via complex interaction between biologically active bacterial molecules and particular targets of signal paths which lead to apoptosis. In intracellular parasitism the apoptosis-suppressing activity of bacteria may be considered to be one of the mechanisms of pathogenic organism's persistence which provide favorable conditions for the development of chronic infections. Infection caused by C. pneumoniae in human fibroblasts has been experimentally demonstrated to protect the cells from spontaneous and induced apoptosis.

[Role of Chlamydia pneumoniae in the etiology of atherosclerosis]. / Rol' Chlamydia pneumoniae v étiologii ateroskleroza.

The review of literature on the role of C. pneumoniae in the etiology of atherosclerosis is presented. The patients with coronary disease show a greater detection rate and higher titers of antibodies to C. pneumoniae. The causative agent can be detected in atheromas in of immunocytochemical studies and by means of electron microscopy, as well as in the polymerase chain reaction. In addition, live C. pneumoniae can be isolated from atheromas. The process of atherogenesis is modeled by infecting susceptible animals with chlamydiae. C. pneumoniae induce the formation of foam cells in the culture of human macrophages due tho the surplus absorption of cholesterol by macrophages from low-density lipoproteins. Chlamydial lipopolysaccharide is capable of inducing the formation of foam cells. The conclusion has been made that C. pneumoniae is one of the possible etiological agents of atherosclerosis. The possible role of the endotoxins of bacteria of the intestinal microflora, regularly supplied to the blood stream in the presence of sharply decreased immunity to endotoxins, in the etiology of atherosclerosis is also supposed.

[Improvement in the method of cultivating Halprowiae (Chlamydiae) in cell cultures]. / Usovershenstvovanie metoda kul'tivnirovaniia gal'provii (khlamidii) v kul'ture kletok.

Comparative evaluation of several methods increasing the effectiveness of cultivating Halprovia (7 strains of different origins) in L-929 and McCoy cell cultures has shown that the maximum effectiveness can be achieved by supplementing the standard method for the cultivation of obligate intracellular parasites with the method of forced adsorption of Halprovia on the monolayer and the treatment of cells with DEAE dextran or cycloheximide. The peculiarities of detecting cytoplasmic halprovian inclusions in infected cells by staining the specimens with fluorescent antibodies, with Lugol's solution, and according to May-Grünwald-Giemsa are described.

[Role of Chlamydia, mycoplasma and cytomegalovirus infection in the development of coronary artery disease]. / Rol' khlamidiinoi, mikoplazmennoi i tsitomegalovirusnoi infektsii v razvitii ishemicheskoi bolezni serdtsa.

AIM: To assess relationship between some infection factors and presence of coronary heart disease. MATERIAL: Patients with myocardial infarction (n=56), unstable angina (n=50), stable angina (n=50) and age - matched controls (n=49). METHODS: Levels of IgG, IgM, IgA antibodies to Chlamydia pneumonia, Chlamydia trachomatis, Chlamydia psittaci, IgG, IgM antibodies to Cytomegalovirus, and also of antibodies and antigen to Mycoplasma pneumoniae were measured in blood serum. RESULTS: Compared with controls patients with coronary heart disease had higher frequency of seropositivity to Chlamydia pneumonia, Mycoplasma pneumonia and Cytomegalovirus (p< 0.05 ) and similar levels of seropositivity to Chlamydia trachomatis and Chlamydia psittaci. Infectious burden (quantity of antibodies per one patient) was significantly higher in patients with myocardial infarction, unstable and stable angina than in controls (1.58, 1.42, 1.41 and 0.95, respectively). CONCLUSION: Our results confirm presence of association between infection and coronary heart disease.