[INTESTINE MICROBIOTA IN CHILDREN WITH OBESITY AND ALLERGIC DISEASES].

AIM: Study intestine microflora in children with obesity and evaluate its association with allergic diseases. MATERIALS AND METHODS. 66 children with various body weight aged 3 to 17 years were included into the study. Intestine microflora study in children was carried out according to the order of the Ministry of Health of Russian Federation No. 231 of 09.06.2003 "Regarding approval of sectoral standard "Patient management protocol. Intestine dysbacteriosis" (SST 91500.11.0004-2003). RESULTS: In healthy children depending on body weight an increase of the number of Firmicutes type microorganisms and a decrease of the number of microbes, belonging to Bacteroidetes type, was detected. The presence of allergic pathology was accompanied by a decrease of the number of Bacteroidetes and the presence of Bacillus and Staphylococcus aureus regardless of the body weight. At the same time, in all the children an increase of the content of Clostridium with the increase of body mass was noted. CONCLUSION. The data obtained have revealed an association of changes in intestine microbiota with the development of obesity and allergopathology.

[Mucosal immune response to Helicobacter pylori in children with gastroduodenal diseases and allergy].

In children with chronic gastritis/gastroduodenitis, erosions and ulcer of stomach and duodenum and associated allergic diseases (asthma, allergic rhinitis, atopic dermatitis) CagA, sIgA and IgE antibodies to the H. pylori were determined by ELISA in the supernatants of feces. H. pylori infection was determined according to "Maastricht IV". The frequency and contents of CagA did not differ among the groups we studied. However, in children with positive urease test the contents of CagA was significantly higher (p = 0.03) compared with other children. The highest levels of sIgA were found in the feces supernatants from non-allergic children with CG/CGD and were associated with H. pylori infection. The immune response in children with erosions and ulcer of stomach and duodenum and in children with allergy was presented the sIgE to H. pylori. Also, the negative correlation between the level sIgE to H. pylori and content sIgA was found in children with allergy. Thus, increased IgE indicates not only allergy, but also acts as a protective role in the development of anti-infective immunity.

[IgE-antibodies to Helicobacter pylori in children with gastroduodenal diseases and concomitant of allergy].

In children with chronic gastritis/gastroduodenitis (CG/CGD), ulcerative and erosive processes of mucous and associated allergic diseases IgM, IgA, IgG, and IgE to the H. pylori were determined by ELISA in the blood serum. IgM-antibodies to H. pylori were found in isolated cases and did not present a diagnostic significance. IgG-antibodies were detected in all children in the same percentage (40-50%), pointing indirectly to the widespread contamination by H. pylori. IgA-antibodies to H. pylori with high frequency (83% and 57%) were found in the blood serum of children with the diseases of gastroduodenal zone without allergies, while in children with allergic pathology they were found by 3-4 times less (20%). IgE antibodies to H. pylori were determined in a high percentage of cases in healthy children (86%) and allergic children (75%), while children without allergy IgE antibodies were detected in the 54-65% of cases. In this study, the detection of IgE antibodies to H. pylori has allowed to increase the frequency of the diagnosis of helicobacteriosis cases in children with gastropathology by 16% in general and in the group of children with allergic diseases this increase amounted to 27.3%. Moreover, children with antihelicobacterial IgE antibodies in a large percentage of cases (92-94%) revealed a positive urease activity. Detection of serum IgE-antibodies to H. pylori in combination with other antibodies isotypes in children increases the diagnostic significance of determination of H. pylori infection and may be recommended when applying serodiagnosis H. pylori in children's practice, especially in children with allergic pathology.

[Evaluation of the interferon system and major cytokines in patients with bronchial asthma].

AIM: Study of the interferon system (IFN) and the production of major cytokines in patients with bronchial asthma of various course severity. MATERIALS AND METHODS: 204 patients with atopic bronchial asthma (BA); 32 patients with allergic rhinitis (AR) and 93 mostly healthy volunteers were examined. Blood cells of patients with BA of various course severity were studied by biological method in HEP cell culture for the ability to produce IFN. Levels of cytokines in the blood sera were determined by EIA method with the corresponding commercial test systems: IL-4, IL-10, IL-13 and IFN-gamma according to user manual. RESULTS: Disorders in the ability ofleukocytes to produce IFN-alpha and IFN-gamma were detected in patients with bronchial asthma and allergic rhinitis. Misbalance in the production of pro- and anti-inflammatory cytokines depending on the level of disease severity was noted. The highest serum IFN-gamma was noticed in patients with mild persistence BA course, that is most probably determined by higher frequency of ARVI in this group of patients. Maximum level of IL-10 was detected in mild BA form and was nearly undetected in the severe course of the infection, which is characterized by higher content of IL-4 in blood sera. CONCLUSION: Increase of course severity of chronic (allergic) inflammation in bronchial tissue and higher frequency of ARVI among patients with persistent BA of medium and severe course is characterized by a lack of interferon link of the immune system and disorders of regulatory mechanisms, that is expressed by a change in the ratio of IFN-gamma/IL-4 parameters and decrease of IL-10 content in blood sera.

Oct-1 is responsible for the C-33T polymorphism effect in the IL-4 promoter.

IL-4 is a pleiotropic immunoregulatory cytokine secreted by Th2 subset of CD4(+) Th cells. Several transcription factors (TFs) have been determined with various degrees of certainty to bind the IL-4 promoter and to regulate its expression in human. To investigate the mechanisms responsible for phenotypic effects of the C-33T IL-4 promoter polymorphism, we performed a search of TFs binding to this promoter locus and discriminating the -33C and -33T alleles. In silico searches suggest few factors bind this region. Using an electromobility shift assay we found that Jurkat T cells contained proteins which specifically interacted with oligonucleotide probes, corresponding to the -33 region. Considerable binding differences between C and T alleles were demonstrated using competitive conditions, the proteins bound predominantly with -33C allele. We found that the transcription factor Oct-1 produced the major shifted complex. The binding of Oct-1 was not improved using activated nuclear extracts; however, we observed increases in other shifted complexes upon cell activation. We suppose that Oct-1 occupancy may compete for binding of activator proteins to closely or overlapped binding sites. Our findings suggest that the interplay between Oct-1 and unknown TFs may be responsible for the C-33T polymorphism effects.