幽门螺杆菌感染的密度和在胃黏膜层不同深度的定植对其致病性和抗生素耐药的影响

Helicobacter pylori infection density and colonization depth in gastric mucosa: Influence on pathogenicity and drug resistance

目的:观察幽门螺杆菌(Helicobacter pylori,H.pylori)在胃黏膜的感染密度及在胃黏膜层不同深度的分布定植对胃黏膜炎症的影响,探讨H.pylori生物膜在其致病性及对抗生素产生耐药机制中的作用.方法:组织病理学观察158例H.pylori阳性慢性胃炎或消化性溃疡患者的胃黏膜病变活检标本,应用苏木精-伊红染色对胃黏膜炎症程度及活动程度分级并观察H.pylori感染密度,比较两者的相关性.应用免疫组织化学染色观察H.pylori在黏膜表面、胃小凹及浅层腺体的分布,比较胃黏膜层不同深度H.pylori定植情况及其感染密度与炎症的关系.结果:免疫组织化学染色显示H.pylori定植在胃黏膜层表面、小凹及浅层腺体.158例胃黏膜组织,黏膜表面H.pylori(+)41例、(++)38例、(+++)79例;小凹(+)29例、(++)42例、(+++)74例;浅层腺体(+)51例、(++)51例、(+++)39例.胃黏膜表面及小凹H.pylori密度与黏膜炎症程度有相关性(P<0.05);浅层腺体H.pylori密度与黏膜炎症程度无明显相关性(P>0.05).158例胃黏膜组织,黏膜表面H.pylori(+)40例、(++)39例、(+++)79例;小凹(+)29例、(++)41例、(+++)74例;浅层腺体(+)48例、(++)53例、(+++)29例.胃黏膜层表面、小凹及浅层腺体H.pylori密度与胃黏膜炎症活动性均有相关性(P<0.05),H.pylori在胃黏膜层不同深度密度越高胃黏膜炎症活动程度越重.结论:H.pylori可以定植在胃黏膜层表面、小凹和浅层腺体,H.pylori感染密度与胃黏膜炎症程度有相关性.具有细菌数量(感染密度)依赖性的H.pylori生物膜可能参与了其致病性及对抗生素的耐药.

AIM： To observe the influence of Helicobacter pylori（H. pylori） infection density and colonization depth in the gastric mucosa on the severity of gastric mucosal inflammation, in order to approach the pathogenicity and the mechanism of antibiotic resistance caused by the H. pylori biofilm.METHODS： Gastric mucosal biopsy specimens were histopathologically studied in 158 patients with H. pylori positive chronic gastritis and peptic ulcer. The severity of gastric mucosa inflammation and the H.pylori infection density were evaluated using haematoxylin-eosin staining to explore the relationship between H. pylori infection density and the severity of gastric mucosa inflammation. The colonization of H. pylori in different layers of the gastric mucosa（gastric mucosa surface, gastric pits, and superficial glands） was observed by immunohistochemistry. The relationship between the H. pylori colonization depth and the severity of gastric mucosa inflammation was analyzed statistically.RESULTS： H. pylori can colonize at the surface, pits and superficial glands of the gastric mucosa as revealed by immunohistochemistry. Of 158 gastric mucosa specimens, 41 had low H. pylori density（＋） at the surface of the gastric mucosa, 38 had moderate H. pylori density（＋＋）, and 79 had high density（＋＋＋）; the corresponding figures were 29, 42 and 74 at the pits, and 51, 51 and 39 at the superficial glands. There was a significant association between H. pylori density and the inflammatory severity at the surface and pits（P〈0.05）, but not at the superficial glands（P〈0.05）. Of 158 gastric mucosa specimens, 40 had low H. pylori density（＋） at the surface of the gastric mucosa, 39 had moderate H. pylori density（＋＋）, and 79 had high density（＋＋＋）; the corresponding figures were 29, 41 and 74 at the pits, and 48, 53 and 29 at the superficial glands. There were significant associations between H. pylori density and inflammatory activity at the surface, pits, and superficial glands（P〈0.05）. Higher H. pylori density was associated with more severe mucosal inflammation.CONCLUSION： H. pylori can colonize at the surface, pits and superficial glands of the gastric mucosa layer. There is a significant association between H. pylori infection density and the severity of gastric mucosa inflammation. H. pylori biofilm, which is formed depending on bacterial number（infection density）, may participate in the pathogenicity and antibiotics resistance of H. pylori.