Can a fungal toxin worsen stomach changes caused by H. pylori in gerbils?

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Helicobacter pylori is a human gastric carcinogen. Sterigmatocystin (ST), a fungal toxin, is a risk factor for gastric cancer. Cytotoxin-vacuolation toxin A (VacA), present in the supernatants of H. pylori suspensions, can cause gastritis and ulcers. This study examined the effects of H. pylori, ST and VacA in Mongolian gerbils.

In this animal exposure experiment, 196 male Mongolian gerbils were given H. pylori supernatants (10 ml/1000 mg) mixed with their diet, or were inoculated intragastrically with H. pylori alone or with ST (100 or 1000 ppb). They were killed 27 months later. Gastric tissue sections were stained with haematoxylin and eosin (H&E), periodic acid-Schiff (PAS), and Alcian blue (AB, pH 2.5), and immunostaining was used to assess PCNA and p53 expression.

In H. pylori-infected gerbils, normal gastric mucosa was replaced by hyperplastic epithelium. Severe gastritis, cystic dilatation of gastric glands, hyperplastic polyps and intestinal metaplasia were observed. Intestinal metaplasia was significantly more frequent in the H. pylori + ST (1000 ppb) group than in animals receiving H. pylori alone. No pathological changes were observed in the H. pylori supernatant group. Osseous metaplasia was observed in the H. pylori + ST (100 ppb) group.

Serum gastrin levels in the H. pylori + ST (1000 ppb) group were significantly higher than in the other groups. The PCNA labelling index and p53 index were significantly higher in infected gerbils than in uninfected groups.

The authors concluded that H. pylori causes gastritis, ulcers and intestinal metaplasia, and that ST enhances the development of intestinal metaplasia and increases gastrin levels in H. pylori-infected Mongolian gerbils.