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Aim. To assess the immune status in children of primary school age with functional disorders of the respiratory system, who live in the territory with location of industrial enterprise, producing aluminium. Materials and methods. Fifty-two children aged 711 years with respiratory system disorders, who live in the zone of exposure of aluminium-producing enterprise were examined. Cellular differentiation marker CD127, protein Bcl-2 and TNFR receptor expression levels were identified using the method of flow cytometry. Phagocytic activity of the cells was studied using formalinized sheep erythrocytes; IgG content was determined with radial immunodiffusion method; beta2-microglobulin level with enzyme immunoassay. Functional status of respiratory system was assessed using spirometry, rhinomanometry methods but functional reserves with calculated Skibinskaya index. Results. The prevalence of allergic diseases in the examined children was 2,4 times higher and allergic rhinitis was diagnosed 3,2 times more often than in the group of comparison. The prevalence of bronchial asthma, clinical signs of chronic lympho-proliferative diseases reliably exceeded the level observed in children of comparison group (29.4 %, р = 0.001). There were established the changes in immune reactivity versus the comparison group, manifested by increase in percentage of phagocyting cells, beta2-microglobulin protein, IgG, CD127, TNFR and specific IgG to aluminium by 1.1, 1.2, 1.0, 1.7, 2.5 and 1.2 times, respectively; suppression of protein Bcl-2 expression by 2,6 times (p 0.05) was registered. Conclusions. Among children aged 711 years, who live in the territory with localized aluminium-producing enterprise, the diseases of respiratory organs with allergic component, reliably associated with aluminium compound contamination, were diagnosed more often than in children of comparison group. Immunologic study detected imbalance between humoral and cellular components of immunity: hyperproduction of specific IgG to aluminium, excess expression of proteins and beta2-microglobulin receptors, IgG, CD127, TNFR and deficit of Bcl-2.

We studied the role of the carrier status for polymorphic loci of genes encoding estrogen receptors (ESR1), endothelial NO synthase (eNOS), and apolipoprotein E (APOE4) and products of their expression nitrogen oxide (NO) and apolipoprotein (ApoE) in the development of arterial hypertension in men. Conventionally healthy volunteers and 149 men with clinical manifestations of stage I-II arterial hypertension were examined. In men with arterial hypertension, the frequency of minor allele A of ESR1 gene was higher (27.5 vs. 9.5% in the reference group; χ=4.43, p=0.04). The level of NO in the peripheral blood was also higher in the main group (χ=3.93, p=0.047). The increase in NO concentration did not depend on the presence of polymorphic genotypes (GG and GT) of eNOS gene, but the decrease in ApoE level in blood serum was associated with TC genotype of APOE4 gene (p=0.04). Our results suggest that minor allele A of ESR1 gene is associated with the development of arterial hypertension in men. Reduced content of ApoE in blood serum of men with arterial hypertension was associated with APOE4 gene polymorphism. However, increased level of NO did not depend on polymorphic genotypes GG and GT of eNOS gene. These polymorphisms are of specific interest as additional markers of genetic predisposition to the development of arterial hypertension in middle-age men.