1,721,345 research outputs found
Are Helicobacter pylori differences important in the development of Helicobacter pylori-related diseases?
No full textHelicobacter pylori colonises the stomach of man and induces a strong mucosal inflammation and a local and systemic immune response. Differences in virulence characteristics of Helicobacter pylori isolates can account for different clinical outcomes of infection. Most determinants of Helicobacter pylori pathogenicity factors are present in all isolates examined; some are present only in or expressed more intensively by certain strains. Many enzymes, i.e., urease, mucinase, phospholipases, alcohol dehydrogenase, neuraminidase, etc. could promote tissue erosion and ulceration by destroying the integrity of mucous, by inducing lipid peroxidation, etc. Strains which express the vacuolating toxin VacA and the associated protein CagA are called Type I and are considered endowed with increased ulcerogenic and inflammatory potential. Type I Helicobacter pylori strains carry a 40 kb genomic fragment called cag which is absent in Type II strains (VacA and CagA negative), and which contains numerous genes encoding for protein homologues to virulence factors expressed by other bacterial pathogens. CagA positive strains are more likely to be isolated from patients with duodenal ulcer and other severe digestive diseases. A simple serological test can help to detect patients at increased risk of developing severe gastroduodenal diseases, which can, therefore, possibly be prevented
Helicobacter pylori exotoxins and gastroduodenal diseases associated with cytotoxic strain infection
No full textHelicobacter pylori factors involved in the development of gastroduodenal mucosal damage and ulceration
No full textMany putative virulence determinants of Helicobacter pylori are believed to trigger and worsen the gastroduodenal mucosa damage observed in infected patients. H. pylori urease reacts with the gastric urea and generates ammonia; ammonia combines with water and yields ammonium hydroxide, which is cytotoxic. Ammonia may also inhibit cell proliferation and cause indirect mucosal injury by stimulating neutrophils. Phospholipases may damage the gastric mucosa by degrading phospholipids and generating precursors of ulcerogenic components. Other enzymes, such as protease, neuraminidase, fucosidase, and alcohol dehydrogenase, can contribute to damage of the gastric epithelium by destroying the integrity of mucus or by inducing lipid peroxidation. Infection by vacuolating cytotoxic (VacA+) H. pylori strains is considered to constitute increased risk for development of peptic ulcer and gastric cancer. Exploration of the vacA gene structure has shown the existence of strongly toxigenic strains, and has confirmed at the molecular level the increased ulcerogenic potential of VacA+ H. pylori strains. A pathogenicity island called cag has been recently described in Type 1 H. pylori strains (VacA+/CagA+).cag contains the cagA gene (whose expression is associated with toxigenicity) and many genes, some of which are highly homologous to virulence genes of other virulent bacteria, that account for the enhanced pathogenic potential of CagA+ organisms
Differentiation of motile and mesophilic Aeromonas strains into species by means of a CAMP-like factor test
No full textMotile and mesophilic Aeromonas strains can presumptively be differentiated into species in 18 to 24 h by testing the isolates for the production of a CAMP-like factor. Aeromonas hydrophila strains were positive either aerobically or anaerobically, Aeromonas sobria strains were positive only aerobically, and Aeromonas caviae strains were always negative
Bacterial pathogenic factors
No full textHelicobacter pylori expresses a number of putative factors of pathogenicity which could account for the gastroduodenal lesions observed in infected patients. An important factor of pathogenicity is the vacuolating toxin A. Molecular studies have shown a mosaic organisation of the vacA gene signal sequence (s) and middle sequence (m) regions, with type s1/m1 being associated with the highest levels of vacuolating activity of the expressed vacuolating toxin A protein. Vacuolating toxin A protein is secreted as monomers of M(r) 95,000. In-vitro, they organise into polymers of approximately M(r) 700,000 and only oligomers stimulate the production of neutralising antibodies, suggesting that aggregation is not casual. Monomers cleave in two fragments of M(r) 37,000 and 58,000. Both fragments penetrate cells in culture, but only the M(r) 58,000 subunit exerts a biological activity. Most cytotoxic H. pylori strains also express a protein called cytotoxin-associated gene protein A. Cytotoxin-associated gene protein A-positive strains carry genomic regions, called picA and picB, which seem to be responsible for the increased inflammatory potential induced by these organisms. Patients with active gastritis, peptic ulceration, and pre-neoplastic or neoplastic mucosal lesions are mostly infected by vacuolating toxin- and cytotoxin-associated gene A-positive strains. Mucosa-associated lymphoid tissue-associated gastric lymphomas are not associated with the cytotoxin-associated gene protein A status of the infecting organisms. The presence of Lewis(x) blood group antigen on the lipopolysaccharide of H. pylori may play an important role in bacterial attachment and the development of autoimmunity in the host. Other potential pathogenicity factors of H. pylori include urease, neuraminidase, haemolysins, flagella and heat-shock proteins, but the role of these bacterial substances has not yet been fully determined
Culture of Helicobacter pylori in broth, determination of vacuolating activity of bacterial broth cultures and neutralization of the vacuolising activity
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