World J Gastroenterol. 2012 Feb 7;18(5):489-90. doi: 10.3748/wjg.v18.i5.489.
Helicobacter pylori (H. pylori) virulence factors promote the release of various chemoattractants/inflammatory mediators, including mainly the neutrophil-attractant chemokine interleukin-8 and neutrophil-activating protein (NAP), involved in H. pylori-induced gastric pathologies. Co-administration of Chios mastic gum (CMG), which inhibits H. pylori NAP, with an H. pylori eradication regimen might add clinical benefits against H. pylori-related gastric pathologies, but possibly not CMG as main therapy. Although H. pylori NAP and other H. pylori-related cytotoxins [i.e., vaculating cytotoxin (VacA)] appear to play a major role in generating and maintaining the H. pylori-associated gastric inflammatory response and H. pylori NAP is a promising vaccine candidate against H. pylori infection (H. pylori-I), concerns regarding its potential drawbacks, particularly neurogenic ones, due to possible cross-mimicry, should be considered. Possible cross-mimicry between H. pylori NAP and/or bacterial aquaporin (AQP) and neural tissues may be associated with the anti-AQP-4 antibody-related neural damage in multiple sclerosis (MS)/neuromyelitis optica patients. Moreover, the sequence homology found between H. pylori VacA and human Na+/K+-ATPase A subunit suggests that antibodies to VacA involve ion channels in abaxonal Schwann cell plasmalemma resulting in demyelination in some patients. A series of factors have been implicated in inducing blood-brain barrier (BBB) disruption, including inflammatory mediators (e.g., cytokines and chemokines induced by H. pylori-I) and oxidative stress. BBB disruption permits access of AQP4-specific antibodies and T lymphocytes to the central nervous system, thereby playing a major role in multiple sclerosis pathogenesis. Relative studies show a strong association between H. pylori-I and MS. H. pylori-I induces humoral and cellular immune responses that, owing to the sharing of homologous epitopes (molecular mimicry), cross-react with components of nerves, thereby contributing and perpetuating neural tissue damage. Finally, H. pylori NAP also plays a possible pathogenetic role in both gastric and colon oncogenesis.
幽门螺杆菌（H. pylori）的毒力因子促进各种趋化因子/炎症介质的释放，包括主要的中性粒细胞趋化因子白细胞介素 8 和中性粒细胞激活蛋白（NAP），它们参与 H. pylori 诱导的胃病理学。与 H. pylori 根除方案一起使用抑制 H. pylori NAP 的奇欧拉乳香树胶（CMG）可能会为治疗与 H. pylori 相关的胃病理学提供临床益处，但可能不是 CMG 作为主要疗法。尽管 H. pylori NAP 和其他 H. pylori 相关细胞毒素[即空泡细胞毒素（VacA）]似乎在产生和维持 H. pylori 相关的胃炎症反应中起主要作用，并且 H. pylori NAP 是一种有前途的针对 H. pylori 感染（H. pylori-I）的疫苗候选物，但由于可能的交叉模拟，应考虑到其潜在的缺点，特别是神经源性的缺点。H. pylori NAP 和/或细菌水通道蛋白（AQP）与神经组织之间的可能交叉模拟可能与多发性硬化症（MS）/视神经脊髓炎患者的抗 AQP-4 抗体相关的神经损伤有关。此外，在 H. pylori VacA 和人 Na+/K+-ATPase A 亚基之间发现的序列同源性表明，针对 VacA 的抗体涉及轴突后施旺细胞质膜中的离子通道，从而导致一些患者脱髓鞘。一系列因素被认为与诱导血脑屏障（BBB）破坏有关，包括炎症介质（例如，由 H. pylori-I 诱导的细胞因子和趋化因子）和氧化应激。BBB 破坏允许 AQP4 特异性抗体和 T 淋巴细胞进入中枢神经系统，从而在多发性硬化症发病机制中起主要作用。相关研究表明 H. pylori-I 与 MS 之间存在很强的关联。H. pylori-I 诱导体液和细胞免疫反应，由于同源表位（分子模拟）的共享，与神经成分发生交叉反应，从而导致和持续神经组织损伤。最后，H. pylori NAP 也可能在胃和结肠肿瘤发生中发挥致病作用。
