Abstract

Introduction. Helicobacter pylori (Hр) is a helix-shaped bacterium adapted evolutionary to living in the mucoid of stomach. Considered usually as one of the factors in the development of gastritis, peptic ulcer and gastric cancer, but the opposite opinions were also discussed. The aim of this study was to assess levels of serum antibodies to Hp and recombinant CagA in the cohort of working-age Moscow adults. Methods. Commercial ELISA kits “IFA-Helicobacter IgG”© (ZAO EKOlab, Russia) and “HelicoBest-antibodies”© (ZAO Vector-Best, Russia) were applied for the estimation of serum antibodies to Hp and CagA, correspondingly, in the observed cohort (both gender adults, N=319). Results. 85 % of the human cohort (N=271) had positive rates of IgG-antibodies against complex Hp antigen, with lognormal distribution of IgG titers (median 1:688; Q1 - Q3 1:370 - 1:1223) and cut-off value equal to 1:100. 54 % of the human cohort (N=172) were seropositive to recombinant CagA, with the levels of total serum antibodies (IgM, IgA and IgG) from 23 to 129 elisa units (median 87,9; Q1 - Q3 56,7 - 102,5) and cut-off value equal to 18,5 EU. The distribtion of CagA antibody levels was sharply different from lognormal distribution of IgG titers to complex Hp antigen and had signs of bimodality with the main maximum shifted to the right. In the complete cohort under observation (N=319), the levels of serum antibodies to Hp and CagA were associated with a weak (R=0,217), but highly significant (p=0,00009) positive linkage; human persons, seropositive to both antigens, had no any association between the markers. Discussion. Possible reasons of differences in the shape of distributions of the studied markers are discussed. Taking into account the extraordinary genetic variability of natural Hp isolates, lognormal distribution of antibodies to complex Hp antigen can reflect combinatorial differences in the degree of proximity of Hp antigenic determinants between human persons under observation and the antigenic preparation. Bimodal distribution of antibody levels to individual protein CagA, possibly, reflect genetically determined differences in immunoreactivity inside the observed cohort.

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