PMC:3091627 / 2569-3873 JSONTXT

{"project":"2_test","denotations":[{"id":"20537153-12197905-10781712","span":{"begin":175,"end":176},"obj":"12197905"},{"id":"20537153-9135515-10781713","span":{"begin":348,"end":349},"obj":"9135515"},{"id":"20537153-3385767-10781714","span":{"begin":531,"end":532},"obj":"3385767"},{"id":"20537153-15759043-10781715","span":{"begin":682,"end":683},"obj":"15759043"},{"id":"20537153-9430586-10781716","span":{"begin":817,"end":818},"obj":"9430586"},{"id":"20537153-12142529-10781717","span":{"begin":827,"end":829},"obj":"12142529"},{"id":"20537153-12377603-10781718","span":{"begin":838,"end":840},"obj":"12377603"},{"id":"20537153-19545429-10781719","span":{"begin":849,"end":851},"obj":"19545429"},{"id":"20537153-15716466-10781720","span":{"begin":971,"end":973},"obj":"15716466"},{"id":"20537153-15557006-10781721","span":{"begin":1070,"end":1072},"obj":"15557006"},{"id":"20537153-16027366-10781722","span":{"begin":1073,"end":1075},"obj":"16027366"},{"id":"20537153-11865403-10781723","span":{"begin":1300,"end":1302},"obj":"11865403"}],"text":"Since the discovery of H. pylori, several studies have focused on elucidating H. pylori pathogenicity mechanisms (microbial factors) that are associated with disease outcomes[5]. The cag-pathogenicity island (cagPAI) has been recognized as a major pro-inflammatory actor, but its association with MALT lymphoma strains has yet to be clearly shown [6]. The VacA vacuolating cytotoxin, thought to cause detectable alterations in gastric epithelial cells and immune cells, is also one of the most studied H. pylori virulence factors [7]. VacA has also been suggested to play a role in H. pylori persistence, demonstrated by in vitro studies, based on its immunosuppressive properties [8]. Adhesion of H. pylori to gastric epithelial cells is another bacterial trait contributing to chronic state of the infection. BabA [9], SabA [10], HopZ [11], HomB [12] and 30 outer-membrane-like paralogs recognized as adhesins or potential adhesins are encoded by the H. pylori genome [13]. Several studies have highlighted their contribution to pathogen fitness in human populations [14,15]. Over the last twenty years, genes encoding these virulence factors have served as genotyping markers to establish correlations between these markers, alone or in combination, and clinical outcomes of H. pylori infections [16]."}