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EN
Helicobacter pylori (H. pylori) bacteria are human pathogens causing symptomatic gastritis, peptic ulcer or gastric cancer. Little is known about the kinetics of immune responses in H. pylori infected patients because the initial moment of infection has not been identified. Various animal models are used to investigate the immune processes related to H. pylori infection. In this study we checked whether H. pylori infection in guinea pigs, mimicking natural H. pylori infection in humans, resulted in the development of specific immune responses to H. pylori antigens by measuring the proliferation of lymphocytes localized in mesenteric lymph nodes, spleen and peripheral blood. The maturity of macrophages and cytokines, delivered by monocyte-macrophage lineage or lymphocytes, were considered as mediators, which might influence the lymphocyte blastogenic response. The obtained results showed the activation of T cells localized in mesenteric lymph nodes by H. pylori antigens in H. pylori infected guinea pigs four weeks postinfection. The blastogenic activity of lymphocytes was shaped by their interaction with antigen presenting cells, which were present in the cell cultures during the whole culture period. Moreover, the balance between cytokines derived from adherent leukocytes including interleukin 8 - IL-8 as well as interferon gamma - IFN-γ, and transforming growth factor beta - TGF-β delivered by lymphocytes, was probably important for the successful proliferation of lymphocytes. The H. pylori specific lymphocytes were not propagated in peripheral blood and spleen of H. pylori infected animals. The modulation of immunocompetent cells by H. pylori antigens or their different distribution cannot be excluded.
EN
Helicobacter pylori is an etiological agent of chronic gastritis, gastric and duodenal ulcers and gastric cancers. The use of an appropriate animal model for experimental studies on the pathogenesis of H. pylori infections is necessary due to the chronic character of such infections and difficulties in identifying their early stage in humans. The aim of this study was to develop a guinea pig model of H. pylori infection and identify its microbiological, histological, serological and molecular determinants. Guinea pigs were inoculated per os with H. pylori strains: CCUG 17874 or ATCC 700312, both producing vacuolating cytotoxin A (VacA) and cytotoxin associated gene A (CagA) protein, suspended in Brucella broth with fetal calf serum (FCS) and Skirrow supplement of antibiotics. To determine H. pylori colonization, 7 and 28 days after the challenge, a panel of diagnostic methods was used. It included culturing of microorganisms from the gastric tissue, histopathological analysis of gastric sections, stained by Mayer,s haematoxylin and eosin to assess inflammatory response, by Giemsa as well as Warthin-Starry silver staining to visualise Helicobacter-like organisms (HLO) and with anti-Ki-67 antigen to assess epithelial cell proliferation. H. pylori infection was also confirmed by polymerase chain reactions (PCR) for detection in gastric tissue of ureC and cagA genes and by serological assessment of H. pylori antigens in faeces. This study showed the usefulness of microbiological, histological, immunological and molecular methods for the detection of persistent H. pylori infections in guinea pigs, which could be an appropriate model for studying H. pylori pathogenesis and the related immune response against these microbes.
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