数据表明，缺铁可增强幽门螺旋杆菌毒力，它可作为一个可测定的生物标记，用来识别具有得胃癌高风险的感染者。

　　胃腺癌与幽门螺旋杆菌感染强相关，但大多数被感染的人不会得胃癌。幽门螺杆菌菌株包含胞嘧啶-腺嘌呤-鸟嘌呤致病基因组（CAG +），它可以编码CagA蛋白和IV型分泌系统（T4SS），从而引发更严重的疾病。幽门螺旋杆菌感染也与缺铁性贫血相关，这同样增强患胃癌危险。

　　为了定义在胃癌进展中，缺铁对微生物的毒性作用，研究人员对维持缺铁的饮食并感染致癌的幽门螺旋杆菌CAG+菌株的蒙古沙鼠展开研究。研究结果显示：铁加速了幽门螺旋杆菌引起的癌前病变和恶性病变的cagA基因依赖性。采集自铁缺乏沙土鼠或生长于铁限制环境中的幽门螺杆菌菌株表现出毒力增强，可以诱导炎症因子。

　　Published December 21, 2012

　　Received for publication April 20, 2012, and accepted in revised form September 27, 2012.

　　Gastric adenocarcinoma is strongly associated with Helicobacter pylori infection; however, most infected persons never develop this malignancy. H. pylori strains harboring the cag pathogenicity island (cag+), which encodes CagA and a type IV secretion system (T4SS), induce more severe disease outcomes. H. pylori infection is also associated with iron deficiency, which similarly augments gastric cancer risk. To define the influence of iron deficiency on microbial virulence in gastric carcinogenesis, Mongolian gerbils were maintained on iron-depleted diets and infected with an oncogenic H. pylori cag+ strain. Iron depletion accelerated the development of H. pylori–induced premalignant and malignant lesions in a cagA-dependent manner. H. pylori strains harvested from iron-depleted gerbils or grown under iron-limiting conditions exhibited enhanced virulence and induction of inflammatory factors. Further, in a human population at high risk for gastric cancer, H. pylori strains isolated from patients with the lowest ferritin levels induced more robust proinflammatory responses compared with strains isolated from patients with the highest ferritin levels, irrespective of histologic status. These data demonstrate that iron deficiency enhances H. pylori virulence and represents a measurable biomarker to identify populations of infected persons at high risk for gastric cancer.

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