[The role of immune factors in the progression of chronic kidney diseases in HIV infection].

AIM: To determine the significance of immune factors in the pathogenesis of kidney injuries in HIV infection, by investigating the cellular and cytokine components of an immune response. MATERIALS AND METHODS: Thirty HIV-infected patients (mean age 31.7±6.2 years) with chronic kidney disease (CKD) were examined. A comparison group consisted of 10 HIV-infected patients without signs of kidney injury. A control group included 24 healthy individuals to analyze immune status and 15 people to estimate the normal values of the cytokine composition. The cellular composition of lymphocytes on a typical immunogram was determined on a flow cytofluorometer; the serum concentrations of cytokines were measured on a multichannel photometer. RESULTS: The HIV-infected patients with kidney injury displayed significant reductions in the absolute (0.2·109/l and 0.4·109/l, respectively; р=0.015) and relative (14.75 and 22%, respectively; р=0.005) counts of CD3+/CD4+ cells and in the immunoregulatory index (0.2 and 0.4, respectively; р=0.014) as compared to those in HIV-infected patients without kidney disease (р≤0.05) with a rise in the number of cytotoxic T cells (CD3+/CD8+). The HIV-infected patients showed a preponderance of immunosuppressive cytokine compositions, as indicated by the high levels of transforming growth factor-ß (a more than 50-fold increase) and by a statistically significant rise in the level of tumor necrosis factor-α (TNF-α) (with CD4+ lymphocyte counts more or less than 200 cells/µl - 19.0 and 24.2 pg/ml, respectively; p=0.017; with HIV RNA levels more and less than 100,000 copies/ml - 24.4 and 19.7 pg/ml, respectively; p=0.012). CONCLUSION: The HIV-infected patients with CKD developed kidney injury in the presence of a more pronounced decrease in blood T helper lymphocyte subpopulation levels with a predominance of proinflammatory and immunosuppressive responses. TNF-α in combination with immunosuppression and high viral loads was established to play a leading role in the development of kidney injury in HIV infection.

[The changes of plasma levels of soluble TNF-alpha and TNF-R1 ratio is a prognostic marker and key element of the stroke pathogenesis].

The goal of the present study was to investigate the plasma levels of sTNF-alpha, sTNF-R1 in acute stroke patients, to study the relation between ones, the neurological stroke severity and functional disability. The investigations comprised 60 ischemic stroke patients, 25 patients form control group. Plasma levels of sTNF-alpha, sTNF-R1 were detected by means of ELISA. The conclusion of interaction of sTNF-alpha and tmTNF-R1 increases inflammatory and apoptotic brain tissue damage on the first day of stroke is drawn. On the 7-th and 21-st days of stroke sTNF-alpha realize a neuroprotective effect. The interaction sTNF-alpha and sTNF-R1 blockade of damage expansion. As the result, prognostic significance of sTNF-alpha/sTNF-R1 is showed.

[To the Fas-induced neurons apoptosis mechanisms in stroke pathogenesis].

The goal of the present study was to investigate the plasma levels of proteins regulating Fas-induced apoptosis in acute stroke and to relate ones to brain damage and clinical features. By means of ELISA soluble Fas receptor (sFas) and soluble Fas ligand (sFasL) plasma levels were detected. Fas protein (CD95) expression on CD3 lymphocytes surfaces was detected using flow cytometry. It is summarized, that Fas-induced apoptosis play significant role in stroke pathogenesis. As the result, prognostic significance of sFasL plasma level is showed. Fas induced apoptosis mechanisms seems to be perspective target for search new therapy stroke patients.