Sgouras Dionyssios N, Panayotopoulou Effrosini G, Martinez-Gonzalez Beatriz, Petraki Kalliopi, Michopoulos Spyros, Mentis Andreas
Dept. of Medical Microbiology, Institut Pasteur Hellenique, 127 Vas. Sofias Avenue, 115 21 Athens, Greece.
Clin Diagn Lab Immunol. 2005 Dec;12(12):1378-86. doi: 10.1128/CDLI.12.12.1378-1386.2005.
In clinical settings, Lactobacillus johnsonii La1 administration has been reported to have a favorable effect on Helicobacter pylori-associated gastritis, although the mechanism remains unclear. We administered, continuously through the water supply, live La1 to H. pylori-infected C57BL/6 mice and followed colonization, the development of H. pylori-associated gastritis in the lamina propria, and the levels of proinflammatory chemokines macrophage inflammatory protein 2 (MIP-2) and keratinocyte-derived cytokine (KC) in the serum and gastric tissue over a period of 3 months. We documented a significant attenuation in both lymphocytic (P=0.038) and neutrophilic (P=0.003) inflammatory infiltration in the lamina propria as well as in the circulating levels of anti-H. pylori immunoglobulin G antibodies (P=0.003), although we did not observe a suppressive effect of La1 on H. pylori colonizing numbers. Other lactobacilli, such as L. amylovorus DCE 471 and L. acidophilus IBB 801, did not attenuate H. pylori-associated gastritis to the same extent. MIP-2 serum levels were distinctly reduced during the early stages of H. pylori infection in the La1-treated animals, as were gastric mucosal levels of MIP-2 and KC. Finally, we also observed a significant reduction (P=0.046) in H. pylori-induced interleukin-8 secretion by human adenocarcinoma AGS cells in vitro in the presence of neutralized (pH 6.8) La1 spent culture supernatants, without concomitant loss of H. pylori viability. These observations suggest that during the early infection stages, administration of La1 can attenuate H. pylori-induced gastritis in vivo, possibly by reducing proinflammatory chemotactic signals responsible for the recruitment of lymphocytes and neutrophils in the lamina propria.
在临床环境中，据报道，给予约氏乳杆菌La1对幽门螺杆菌相关性胃炎有积极作用，但其机制尚不清楚。我们通过供水系统持续给幽门螺杆菌感染的C57BL/6小鼠投喂活的La1，并在3个月的时间里跟踪其定植情况、固有层中幽门螺杆菌相关性胃炎的发展以及血清和胃组织中促炎趋化因子巨噬细胞炎性蛋白2（MIP-2）和角质形成细胞衍生细胞因子（KC）的水平。我们记录到固有层中淋巴细胞（P = 0.038）和中性粒细胞（P = 0.003）的炎性浸润以及循环中抗幽门螺杆菌免疫球蛋白G抗体水平（P = 0.003）均显著减轻，尽管我们未观察到La1对幽门螺杆菌定植数量的抑制作用。其他乳杆菌，如解淀粉乳杆菌DCE 471和嗜酸乳杆菌IBB 801，对幽门螺杆菌相关性胃炎的减轻程度不如La1。在La1处理的动物中，幽门螺杆菌感染早期血清MIP-2水平明显降低，胃黏膜中MIP-2和KC水平也降低。最后，我们还观察到，在存在经中和（pH 6.8）的La1废弃培养上清液的情况下，体外人腺癌AGS细胞中幽门螺杆菌诱导的白细胞介素-8分泌显著减少（P = 0.046），且幽门螺杆菌活力未随之丧失。这些观察结果表明，在感染早期，给予La1可在体内减轻幽门螺杆菌诱导的胃炎，可能是通过减少负责募集固有层中淋巴细胞和中性粒细胞的促炎趋化信号来实现的。
