Nowa wersja platformy, zawierająca wyłącznie zasoby pełnotekstowe, jest już dostępna.
Przejdź na https://bibliotekanauki.pl
Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 6

Liczba wyników na stronie
first rewind previous Strona / 1 next fast forward last
Wyniki wyszukiwania
Wyszukiwano:
w słowach kluczowych:  HELICOBACTER PYLORI
help Sortuj według:

help Ogranicz wyniki do:
first rewind previous Strona / 1 next fast forward last
EN
Helicobacter pylori is now recognized as the major causative agent of chronic superficial gastritis in humans. The virulence factors of H. pylori are still poorly understood. Vacuolating cytotoxin (VacA) is one of the factors that has been identified so far. VacA induces cytoplasmic vacuolation in eukaryotic cells. The vacA gene encodes a precursor protein of 140 kDa which consists of a 33-amino acid signal sequence, the 87 kDa cytotoxin and a 50 kDa C-terminal domain. The 50 kDa domain is involved in translocation of VacA across outer membrane. Sequence analysis of vacA gene derived from different strains of H. pylori revealed the existence of several families of vacA gene allels. Analysis of a clinically isolated strains of H. pylori showed the correlation between presence of specific vacA allels, VacA activity and peptic ulceration
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.
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
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
The cure rates of Helicobacter pylori infection by using a combination of a proton pump inhibitor (PPI) and antimicrobial agents are mainly influenced by bacterial susceptibility to antimicrobial agents and the magnitude of acid inhibition during the treatment. Currently used empirical triple therapies do not reliably produce a 80% cure rate on an intention-to-treat basis. Therefore, tailored regimens based on relevant microbiological findings and pharmacogenomics are recommended for attaining an acceptable 95% cure rate. Recently, virulence factors of H. pylori, such as cagA and vacA, are reported to be major factors determining the cure rates. Individuals infected with strains with cagA-negative and vacA s2 genotypes have significantly increased risk of eradication failure of H. pylori infection. These virulence factors enhance gastric mucosal inflammation and are associated with the development of peptic ulcer and gastric cancer. H. pylori virulence factors induce proinflammatory cytokines, such as interleukin (IL)-1, IL-8, and tumor necrosis factor (TNF)-?, which influence mucosal inflammation and/or gastric acid secretion. When physicians select an H. pylori eradication regimen with an acceptable cure rate, they might need to consider H. pylori virulence factors, especially cagA and vacA.
EN
Helicobacter pylori is a Gram-negative, spiral-shaped pathogenic bacterium that was firstly isolated and cultured from biopsy specimens by Marshall and Warren in 1983.This organism is a human gastric pathogen associated with peptic ulcer disease as well as chronic gastritis. Recent epidemiological studies have demonstrated that H. pylori is a primary risk factor for the development of intestinal type gastric adenocarcinoma. H. pylori is the first bacterium for which the genomes of two unrelated strains (26695 and J99) have been sequenced. The genome of H. pylori is relatively low in size (1.6-1.73 Mb). In this review, we compare the organization of two sequenced H. pylori genomes. A special emphasis on genetic diversity of H. pylori including plasticity zone and cag pathogenicity island has been placed.
first rewind previous Strona / 1 next fast forward last
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.