PATHOLOGY, PATHOPHYSIOLOGY, AND DIAGNOSIS OF HELICOBACTER HEILMANNII INFEDTION

我们回顾了4074例连续接受食管胃十二指肠镜检查的日本患者的胃活检资料，以及15例heilmannii螺杆菌感染（1例慢性胃炎；4例粘膜相关淋巴组织（MALT）淋巴瘤）患者的胃活检资料。在连续的系列中，海氏嗜血杆菌的患病率为0.1%。慢性胃炎患者胃镜下胃黏膜正常（13.3%）、有红斑（33.3%）、糜烂（53.3%）；组织学上未见上皮改变，单核细胞轻度浸润，中性粒细胞轻度局灶性浸润。H.heilmannll抗体呈阳性。幽门螺杆菌抗体，并在黏液凝胶层和小窝中检测到。与此相反，海曼螺杆菌感染患者的血清和尿中幽门螺杆菌抗体检测结果为阴性，提示海曼螺杆菌中存在相对特异性抗原：根除海曼螺杆菌可导致MALT淋巴瘤缓解。海曼氏杆菌感染在日本成年人中并不常见，但与慢性胃炎和胃MALT淋巴瘤有关。蒙古沙鼠模型显示出高发生率的胃MALT淋巴瘤样病变，而蒙古沙鼠感染幽门螺杆菌模型显示出增生性息肉和溃疡。在感染幽门螺杆菌的蒙古沙鼠中，黏膜IL-1β mRNA在感染早期呈高水平表达，在感染4周时达到最高值，随后迅速下降。粘膜IFN-γ mRNA也在第4周达到最高水平，但此后仍保持较高水平。IL-1β和IFN-γ mRNA水平在幽门黏膜均高于基底黏膜。相比之下，IL-4、IL-6和IL-10 mRNA水平在8 ~ 26周达到峰值，并且在幽门黏膜和基底粘膜中水平相似。溃疡沙鼠的IFN-γ mRNA水平显著高于增生性息肉沙鼠。不同的结果（如溃疡或增生性息肉）可能与细胞因子之间的不平衡有关。在蒙古沙鼠中，幽门螺杆菌中virD4基因的缺失暂时延缓了胃炎症，但并没有消除胃炎症，幽门螺杆菌中cage基因的缺失通过降低定植能力部分消除了胃炎症。除CagA外，与IV型分泌系统相关的未知因素也可能影响胃炎症。少

Gastric biopsy materials of 4074 consecutive Japanese patients undergoing esophagogastroduodenoscopy were reviewed, along with those of 15 patients with Helicobacter heilmannii (H.heilmannii) infection (1, chronic gastritis ; four, mucosa-associated lymphoid tissue (MALT) lymphoma]. The prevalence of H.heilmannii was 0.1% in the consecutive series. In chronic gastritis, the gastric mucosa was endoscopically normal (13.3%), had erythema (33.3%), or had erosions (53.3%) ; histologically, it showed no epithelial change, mild mononuclear cell infiltration, and slight and focal neutrophil infiltration. H.heilmannll was positive with anti-H.pylori antibody, and was detected in the mucous gel layer and in foveolae. In contrast, the serum and urinary antibody tests for H.pylori infection produced negative results in patients with H.heilmannii infection, suggesting the presence of relatively specific antigens in H.heilmannii : Eradication of H.heilmannii resulted in remission of MALT lymphoma. … More H.heilmannii infection is uncommon in Japanese adults, but is associated with chronic gastritis and gastric MALT lymphoma. A Mongolian gerbil model exhibited a high incidence of gastric MALT lymphoma-like lesion by H.heilmannii, whereas a Mongolian gerbil model of H.pylori infection exhibited hyperplastic polyps and ulcers. In Mongolian gerbils with H.pylori infection, high levels of mucosal IL-1β mRNA were observed early in the infection, reaching maximum at 4 weeks and then rapidly declining. Mucosal IFN-γ mRNA also reached maximal levels at 4 weeks but remained high there after. Both IL-1β and IFN-γ mRNA levels were consistently higher in the pyloric mucosa than in the fundic mucosa. In contrast, IL-4, IL-6, and IL-10 mRNA levels peaked at 8 to 26 weeks and levels were similar in the pyloric mucosa and the fundic mucosa. IFN-γ mRNA levels were significantly higher in gerbils with ulcers than in those with hyperplastic polyps. The different outcomes (e.g., ulcers or hyperplastic polyps) might relate to imbalances among cytokines. In Mongolian gerbils, loss of the virD4 gene in H.pylori temporally retarded but did not abrogate gastric inflammation, and loss of the cage gene in H.pylori abolished gastric inflammation partially via reduced ability to colonize. Unknown factors related to the type IV secretion system other than CagA may influence gastric inflammation. Less