Eck等［24］采用免疫印迹法检测68例MALTomas患者和49例慢性胃炎患者的血清抗-cagA IgG，胃MALTomas患者阳性率达95.5％，而慢性胃炎组阳性率仅67％，提示cagA与胃MALTomas有关。然而，De Jong等［25］用PCR方法检测12例胃MALTomas，38例胃溃疡和39例消化不良患者的胃粘膜活检标本的cagA，三者之间的检出率无统计学意义。故认为感染cagA与胃MALTomas的发生关系不大。Crabtree等［26］认为de Jong等采用的实验方法合适，对照组的分析结果与以前的文献报道相一致。因此，尽管病例样本数较少，但所得到胃MALTomas的发生与cagA+ HP感染关系不大的结论是可信的。
5 cagA-HP引起胃部疾病的可能机理
感染cagA-HP与消化性溃疡高度相关，并且大大增加发生萎缩性胃炎，胃癌的危险性［10，18，20］。尽管相关的原因尚不清楚，但有证据提示cagA+HP引起胃部疾病的可能机理与炎症有关（图1）。与cagA-HP相比，感染cagA+HP患者其胃中HP定植密度（bacterial density）是cagA-HP的5倍多，对胃粘膜上皮造成更大的损伤，增加多形核细胞的浸润，诱导胃上皮细胞分泌过多的炎症因子，如IL-8,IL-Lα，IL-1β［27，11～13］。反复炎症可以刺激胃酸过多的分泌，诱发胃溃疡的发生；同时，胃部炎症引发大量胃上皮细胞的损伤、变性，加速萎缩性胃炎的发展，增加胃癌发生的危险性。另外，cagA+HP感染可激活胃内巨噬细胞活性，导致反应性氧产物（reactive oxygen species,ROS）如O-NO及诱变剂的形成，诱发胃癌的发生。
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