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EN
Helicobacter pylori is recognized as an important cause of chronic antral gastritis and peptic ulceration. Moreover, H. pylori associated inflammatory process has been linked with gastric carcinoma. Many putative virulence factors of H. pylori have been suggested, including motility, urease and cytotoxins production and bacterial adhesins. An accessory function of CagA antigen and bacterial heat - shock proteins in the pathogenesis of H. pylori infections have been also considered. H. pylori - induced immunological response is discussed as regards local and general antibody production, the interaction of the bacteria with the phagocytes and still controversial involvement of T cells. Data on the importance of cytokines and inflammatory mediators in the disruption of the gastric mucosal barriers as well as the evidence to support a role for H. pylori as a risk factor for gastric carcinoma are also presented.
EN
A wide range of techniques was developed for identification of Helicobacter pylori, since the association of the microorganism with gastritis and peptic ulcer has been established in 1983. Up to now, isolation and identification of H. pylori from the gastric biopsy, remains the standard diagnostic procedure. However, attention is focused on rapid no-invasive tests, for monitoring the infection, such as urea breath test. Serological methods as ELISA and Western blot are suitable for estimation of specific anti - H. pylori local and systemic humoral response. Molecular tests based on PCR reaction allow the detection of H. pylori in biopsy specimens and recently in other clinical samples as saliva or faeces. They are also very promissing in epidemiological studies.
EN
Phagocytosis is the critical first step in the Mycobacterium (M.) tuberculosis-phagocyte interaction. The process involves microbial ligands and phagocyte surface receptors. It is known that serum mannose-binding lectin (MBL), an innate immune system component, may enhance the uptake of microbes by phagocytic cells and activate the complement system. Since phagocytes are the replicative environment for mycobacteria and, as we described earlier, tuberculosis patients differ from controls in serum MBL level, we asked whether MBL plays a role in promoting M. tuberculosis access to phagocytic cells. To estimate the influence of MBL on the phagocytic process, FITC-labeled Mycobacterium bovis BCG was used as a model bacterium. Neutrophils from healthy individuals were used as phagocytes. Phagocytosis was performed in the presence or absence of recombinant MBL (rMBL; 2 or 20 g/ml). The activation of complement was determined by dot-blot immune assay with monoclonal antibodies against C5b-C9. We showed that phagocytosis of the bacteria was more intensive in the presence of human rMBL. Both attachment and ingestion of mycobacteria were enhanced when MBL and active complement components (fresh serum) were present in the medium. The dot-blot method showed that the bacteria slightly activated complement by themselves. This effect was enhanced in the phagocyte-bacteria co-cultures containing rMBL.It is possible that MBL may serve in vivo as one of the factors facilitating the entry of mycobacteria into phagocytes, pathogen spread, and the establishment of infection.
EN
Many of H. pylori strains causing gastroduodenal diseases have a cagA gene encoding CagA protein, a virulence factor of these bacteria. Anti-CagA antibodies produced by majority of people infected with CagA(+) strains can indicate such infection. In this study the efficacy of three immunoenzymatic tests: immunoblot (MileniaID Blot H. pylori IgG, DPC Biermann GmbH, Germany) (MB) and ELISA, conducted with a recombinant immunodominant fragment of CagA (rCagA) and full length CagA molecule (flCagA), in detecting CagA(+) and CagA(-) infections, was compared. The 13C urea breath test (13C-UBT) was used for establishing H. pylori status. The serum samples from 157 individuals were used for serodiagnosis. The H. pylori CagA(+) infection was detected in H. pylori infected individuals with similar frequency by MB (64%) and flCagA-ELISA (60%) and little less frequently by rCagA-ELISA (53%). There was a high coincidence between the negative results of these three tests for H. pylori uninfected individuals with no anti-CagA IgG in the serum (96-100%). The results show that rCagA-ELISA and especially flCagA-ELISA are easy, inexpensive and useful noninvasive assays for discrimination of CagA(+) and CagA(-) H. pylori infections in the subjects examined by urea breath test.
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