Resistant gastric environment of Lactobacillus crispatus from stomach inhibits Helicobacter pylori colonization and attenuates gastric inflammation
Abstract Background Recent studies have shown that gastric-derived Lactobacillus can inhibit the colonization of H. pylori and attenuate gastric inflammation in conventional animals, but the resistant of Lactobacillus to gastric environment is still unknown. Here, we aimed to screen the candidate Lactobacillus that could adapt to the harsh gastric environment and inhibit the colonization of H. pylori. Results In vitro, the growth rate of seven Lactobacillus strains in different pH and bile salt concentration were tested, the size of inhibition zone and adhesion rate of H. pylori when Lactobacillus exist were measured. In gnotobiotic mice models, we examined the amount of colonization of L. crispatus and H. pylori by qRT-PCR and evaluated the inflammation in the gastric tissue by the content of MPO and H&E stain. In vitro experiments showed L. crispatus had a better growth rate than other six Lactobacilluses in pH 2.5 to 4.5; under the 0.2% bile salt concentration, other bacteria did not grow except for L. crispatus; L. crispatus yielded 24.2 mm of mean inhibitory zone diameters; the adhesion rate of H. pylori only reached 41.3% in H. pylori-L. crispatus group(HLG). In vivo, the amount of colonization of H. pylori in HLG is fifteen times less than that in H. pylori group (HG) (p < 0.05); the MPO value of HG was 1.4 times that of HLG; the gastric tissue inflammation of HLG was obviously lighter than HG. L. crispatus may be an adjunctive therapy for treating H. pylori- associated disease in clinic. Conclusions L. crispatus has resistance to low acid and high bile salts environment and it inhibits the growth of H. pylori and the subsequent inflammation H. pylori caused in gnotobiotic Kunming mice model, which suggest the potential of developing L. crispatus as clinical agents.