Implicação de genes da zona de plasticidade e da ilha de patogenicidade cag (PAIcag) de Helicobacter pylori no desenvolvimento de doenças gastroduodenais / Implication of Helicobacter pulori plasticity region and cag pathogenicity island (cagPAI) genes on the development of gastroduodenal diseases

Alline Roberta Pacheco

Helicobacter pylori is a Gram-negative, spiral-shaped, flagellated, micro-aerophilic bacterium, included in the Helicobacteraceae family, which infects the human stomach cronically. H. pylori infection has a worldwide distribution and is associated with the development of several gastroduodenal diseases, such as gastritis, peptic ulcer disease (PUD) and its subtypes, gastric ulcer (GU) and duodenal ulcer (DU), and gastric adenocarcinomas. The number of infected individuals are high but only a minority of them will develop serious gastroduodenal diseases. Disease outcome depends on many factors, including host physiology, environmental influences and bacterial genotype. Although a number of putative virulence factors had been reported (cagA, cagE and vacA) for H. pylori, their presence has tipically been associated with an increased risk of both gastric cancer and peptic ulcer disease, and none can be clearly linked to one specific H. pylori related-disease. So the identification of a disease-specific H. pylori virulence factors predictive of the outcome of infection remains unachieved. Several of the H. pylori putative virulence genes that may play a role in its pathogenicity have been identified, many of them located in the cag pathogenicity island (PAIcag) and in the plasticity zone of the H. pylori genome. Data from the literature shows an association between cagT and PUD development, as well as dupA and DU. The latter has been suggested as an universal marker for the development of duodenal ulcers. In this work, we investigated the presence of virB11 and cagT, located in the left half of PAIcag, and the genes jhp917-jhp918, components of the dupA locus, which is located in the plasticity zone region of H. pylori, in brazilian isolates. In addition, we investigated a possible association between these genes and some H. pylori relateddiseases, such as gastritis, PUD, GU, DU and gastroesophageal-reflux (GERD), in an attempt to find a gene marker for a clinical outcome resulted from H. pylori infection. The cagT gene was associated with PUD; virB11 gene was detected in nearly all the samples; dupA locus was not associated with development of DU neither any gastroduodenal disease. In this way, our results suggest that cagT can be used as a marker for the developmentof PUD in State of São Paulo, Brazil; virB11 can be an essential virulence gene for H. pylori pathogenesis on the development of gastritis, PUD and GERD; dupA locus is not an universal marker for the development of DU

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