Abstract

Influenza A(H1N1)pdm09-infection is known to induce exuberant proinflammatory cytokine response in both respiratory and extra-respiratory tissues. Interleukin 10 is a powerful anti-inflammatory factor in intercellular interactions, including the main participants in adaptive cellular and humoral immunity – lymphocytes and platelets (lymphocyte-platelet adhesion). Interleukin 10 contributes to the effective regulation of cellular homeostasis in minimal concentrations. Genetic defects in the genes of anti-inflammatory cytokines can contribute to different production of encoded molecules, which determines the individual characteristics of the course of the infectious process in carriers of polymorphic mutations. The study was performed in 89 patients with influenza A(H3N2) and 96 healthy residents. Gene polymorphism of IL-10 was detected by PCR method. Amplification of IL-10 gene fragments was performed in a thermal cycler (Model “BIS”-M111, Novosibirsk). The percentage of lymphocyte-platelet aggregates (LTA) determined by light microscopy (method of Yu.A. Vitkovsky (1999)). The cytokine level measured by solid-phase ELISA using a set of reagents of Vector-Best (Novosibirsk). The program Statistica 10.0 was used for data processing. Such methods as Equilibrium Hardy-Weinberg, χ2-test and odds ratio descriptive statistics were used. It was found that the chance of developing influenza A(H3N2) increases in persons carrying the allele T 2,18 [CI95 %: 1,33-3,58]) (р=0,002), heterozygous C/T variant (2,88 [СI95 %: 1,56-5,32]) (р=0,002) of the IL-10 gene promoter (C819T) and allele A (4,23 [CI95 %: 2,50-7,14]) (р=0,002), heterozygous G/A (5,60 [CI95 %: 2,84-11,04]) (р=0,001) of the IL-10 gene promoter (G1082A). Among influenza A(H3N2) patients, the C/C and G/G homozygous carriers had the lowest concentration of IL10, while the highest concentration was found in the carriers of the T/T and A/A variants. Carriers of the C/C and G/G genotype of the IL-10 gene promoter (С819Т, G1082A) have the highest ability for lymphocytic-platelet adhesion in influenza A(H3N2).

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