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The indigenous bacterial microbiome of the stomach, including lactobacilli, is vital in promoting colonization resistance againstCandida albicans . However, there are gaps in our understanding aboutC. albicans gastric colonization versus disease, especially during the postantibiotic recovery phase. This study compared the gastric responses toC. albicans strains CHN1 and SC5314 in microbiome-disturbed and germfree mice to elucidate the contribution of the indigenous microbiota inC. albicans colonization versus disease and yeast-bacterium antagonism during the post-cefoperazone recolonization period.C. albicans can prevent the regrowth ofLactobacillus spp. in the stomach after cefoperazone and promote increased colonization byEnterococcus spp. Using a culture-independent analysis, the effects of oral cefoperazone on the gastric bacterial microbiota were observed to last at least 3 weeks after the cessation of the antibiotic. Disturbance of the gastric bacterial community by cefoperazone alone was not sufficient to cause gastritis,C. albicans colonization was also needed. Gastritis was not evident until after day 7 in cefoperazone-treated infected mice. In contrast, in germfree mice which lack a gastric microbiota,C. albicans induced gastric inflammation within 1 week of inoculation. Therefore, the gastric bacterial community in cefoperazone-treated mice during the first week of postantibiotic recolonization was sufficient to prevent the development of gastritis, despite being ineffective at conferring colonization resistance againstC. albicans . Altogether, these data implicate a dichotomy betweenC. albicans colonization and gastric disease that is bacterial microbiome dependent.

Interplay between the Gastric Bacterial Microbiota and Candida albicans during Postantibiotic Recolonization and Gastritis