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10.1111/hel.12251

http://scihub22266oqcxt.onion/10.1111/hel.12251
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C4572604!4572604!26372819
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suck abstract from ncbi

pmid26372819      Helicobacter 2015 ; 20 (0 1): 8-16
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  • Pathogenesis of Helicobacter pylori infection #MMPMID26372819
  • Sgouras DN; Trang TTH; Yamaoka Y
  • Helicobacter 2015[Sep]; 20 (0 1): 8-16 PMID26372819show ga
  • Three decades have passed since Warren and Marshall described the successful isolation and culture of Helicobacter pylori, the Gram-negative bacterium that colonizes the stomach of half the human population worldwide. Although it is documented that H. pylori infection is implicated in a range of disorders of the upper gastrointestinal tract, as well as associated organs, many aspects relating to host colonization, successful persistence and the pathophysiological mechanisms of this bacteria still remain controversial and are constantly being explored. Unceasing efforts to decipher the pathophysiology of H. pylori infection have illuminated the crucially important contribution of multifarious bacterial factors for H. pylori pathogenesis, in particular the cag pathogenicity island (PAI), the effector protein CagA and the vacuolating cytotoxin VacA. In addition, recent studies have provided insight into the importance of the gastrointestinal microbiota on the cumulative pathophysiology associated with H. pylori infections. This review focuses on the key findings of publications related to the pathogenesis of H. pylori infection published during the last year, with an emphasis on factors affecting colonization efficiency, cag PAI, CagA, VacA and gastrointestinal microbiota.
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