Two stomach-originated Lactobacillus strains improve Helicobacter pylori infected murine gastritis

Abstract

Aim: To investigate the potential anti-Helicobacter pylori (H. pylori) and anti-inflammation in vivo effects of two lactobacillus strains from human stomach.

Methods: Forty H. pylori infected Balb/c mice were randomly divided into 4 groups: proton pump inhibitor and antibiotics triple treated group, Lactobacillus fermenti (L. fermenti) treated group, Lactobacillus acidophilus treated group and normal saline control group. Ten uninfected mice were also included as blank control group. The infection of H. pylori was detected by rapid urease tests, Giemsa staining and bacterial culture. The colonization of H. pylori was assessed in bacterial density score and gastric inflammation was assessed in histological score. The colonization of L. fermenti was performed by fluorescent probe.

Results: Histopathologic evaluation showed significant release of mucosal inflammation in gastric antrum and gastric body in lactobacillus treated groups and triple treated group. H. pylori eradication rate in both lactobacillus treated groups and triple treated group were higher than normal saline control group. Lactobacillus treated groups and triple treated group showed significant decrease of H. pylori bacterial density.

Conclusion: Both lactobacillus strains have a significant anti-H. pylori activity; L. fermenti displays more efficient antagonistic activity in vivo against H. pylori infection.

Figure 1

Histological image of gastric antrum and gastric body. A: Histological image of gastric antrum. a: Normal group, normal mucosa, no mucosal erosion; b: NS group, extensive inflammation in the mucosal layer, massive mixed cell infiltration (mainly mononuclear); c: Triple group, slightinflammatory cell infiltration; d: L. fermenti group, a few incomplete mucosa; e: L. acidophilus group, slight inflammation with moderate cell infiltration, (HE, light microscope, × 200); B: Histological image of gastric body. a: Normal group, normal mucosa, no mucosal erosion; b: NS group, extensive inflammation in mucosal layer, even in submucosal layer with massive mixed cell infiltration; c: Triple group, a few incomplete mucosa, slight inflammatory cell infiltration; d: L. fermenti group, almost normal mucosa, slight cell infiltration; e: L. acidophilus group, moderate inflammation with cell infiltration in submucosa (HE, light microscope, × 200).

Figure 2

Histological score of all groups (mean ± SD, n = 10). ^aP < 0.05 vs NS group. The highest score was 2.88 ± 0.38 in gastric antrum and 2.82 ± 0.42 in gastric body in NS group. ^cP < 0.05 vs blank control group.

Figure 3

Bacterial density and bacterial density score of H. pylori. A: Bacterial density of H. pylori. a: Normal group, no detectable H. pylori; b: NS group, over 10 H. pylori were detected in one field of view; c: Triple group; d: L. fermenti group; e: L. acidophilus group, (Giemsa, light microscope, × 1000). B: Bacterial density score of H. pylori. mean ± SD, n = 10. ^aP < 0.05 vs NS group. The highest score was 1.95 ± 0.52 in gastric antrum and 1.88 ± 0.63 in gastric body in NS group.

Figure 4

Fluorescent microscopic detection of L. fermenti labeled with cFDA-SE. A: 2 h, a diffusely distributed cFDA-SE labeled bacteria under fluorescent microscopy; B: 4 h, slightly reduced in comparison with 2 h; C: 8 h, cFDA-SE labeled bacteria reduced obviously; D: Blank control group, no cFDA-SE labeled bacteria was detected.