ارتباط معکوس بین جریزه بیماریزایی CagG هلیکوباکتر پیلوری و خطر زخم معده

عنوان انگليسی

Inverse Relationship Between Helicobacter pylori cagG Pathogenicity Island and Risk of Gastric Ulcer

خلاصه انگلیسی

Helicobacter pylori is a spiral-shaped gram-negative bacterium that infects the human gastric mucosa and is associated with the development of gastrointestinal diseases such as chronic atrophic gastritis, peptic ulceration, and gastric adenocarcinoma. About 10-15% of H.pylori infections have been reported to lead to peptic ulceration, and H.pylori is responsible for 70-85% of gastric ulcers and 90-95% of duodenal ulcers [1]. The cag pathogenicity island (cagPAI)of H. pylori contains some 32 different genes, encoding a type IV secretion system (T4SS). The presence of cagPAI is associated with the development of peptic ulcerations [2,3]. The cagPAI locus has a length of about 40 kb and includes 2 sections: the cagI region containing 16 genes and the cagII region containing 14 genes. The two cagA and cagE genes from the cagI region, and the cagT and cagM genes, as markers of the cagII region, play an important role in gastroduodenal diseases, such as peptic ulceration, gastric cancer [4-6] ,duodenal ulceration and gastric ulceration [9, 10]. CagL and CagH are two other proteins from cagPAI that are essential for transfer and injection of CagA into host epithelial cells as well as formation of T4SS pili [2]. In our hands, the cagL, but not the cagH gene is strongly associated with the risk of peptic ulceration [2], and elsewhere this genotype is associated with the risk of duodenal ulcer [11]. The cagG and orf17 genes are two other genes from cagPAI. The cagG gene is located upstream of the cagA gene and encodes the CagG protein, which plays a role in colonization and inflammation. Although orf17 has no significant relationship with gastric cancer, it is related to the risk of peptic ulceration [2]. Accordingly, pyloric ulcers-related risk factors should be considered separately for duodenal and gastric ulceration. Therefore, we hypothesised an associations betweenf H. pylori cagPAI genotypes (i.e. cagL, orf17, cagG, and cagH) with the risk of either gastric or duodenal ulceration.

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