Erosions and gastroesophageal ulcers (GEU) were produced in the pars esophagea of young gnotobiotic swine fed a carbohydrate-enriched liquid diet and monoinfected with two different fermentative commensal bacteria, Lactobacillus and Bacillus sp. In contrast, piglets, fed a similar diet and inoculated with Gastrospirillum sp. (Helicobacter heilmannii), a helicobacter species that colonizes the gastric mucosa, did not develop GEU. Experimental GEU likely develops secondary to epithelial damage mediated by microbial-origin acids whose production is potentiated by high dietary carbohydrate and parietal cell-origin hydrochloric acid.
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Krakowka et al. (1998) studied this question.
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