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　　數(shù)據表明，缺鐵可增強幽門螺旋桿菌毒力，它可作為一個可測定的生物標記，用來識別具有得胃癌高風險的感染者。

　　胃腺癌與幽門螺旋桿菌感染強相關，但大多數(shù)被感染的人不會得胃癌。幽門螺桿菌菌株包含胞嘧啶-腺嘌呤-鳥嘌呤致病基因組（CAG +），它可以編碼CagA蛋白和IV型分泌系統(tǒng)（T4SS），從而引發(fā)更嚴重的疾病。幽門螺旋桿菌感染也與缺鐵性貧血相關，這同樣增強患胃癌危險。

　　為了定義在胃癌進展中，缺鐵對微生物的毒性作用，研究人員對維持缺鐵的飲食并感染致癌的幽門螺旋桿菌CAG+菌株的蒙古沙鼠展開研究。研究結果顯示：鐵加速了幽門螺旋桿菌引起的癌前病變和惡性病變的cagA基因依賴性。采集自鐵缺乏沙土鼠或生長于鐵限制環(huán)境中的幽門螺桿菌菌株表現(xiàn)出毒力增強，可以誘導炎癥因子。

　　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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