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Ma F, Misumi J, Zhao W, et al. Long-term Treatment with Sterigmatocystin, a Fungus Toxin, Enhances the Development of Intestinal Metaplasia of Gastric Mucosa in Helicobacter pylori-infected Mongolian Gerbils. Scand J Gastroenterol. 2003;38(4):361-369doi: 10.1080/0036552031001699.
Ma, F., Misumi, J., Zhao, W., Aoki, K., & Kudo, M. (2003). Long-term Treatment with Sterigmatocystin, a Fungus Toxin, Enhances the Development of Intestinal Metaplasia of Gastric Mucosa in Helicobacter pylori-infected Mongolian Gerbils. Scandinavian journal of gastroenterology, 38(4), 361-369. https://doi.org/10.1080/0036552031001699
Ma, F, et al. "Long-term Treatment with Sterigmatocystin, a Fungus Toxin, Enhances the Development of Intestinal Metaplasia of Gastric Mucosa in Helicobacter pylori-infected Mongolian Gerbils." Scandinavian journal of gastroenterology vol. 38,4 (2003): 361-369. doi: https://doi.org/10.1080/0036552031001699
Ma F, Misumi J, Zhao W, Aoki K, Kudo M. Long-term Treatment with Sterigmatocystin, a Fungus Toxin, Enhances the Development of Intestinal Metaplasia of Gastric Mucosa in Helicobacter pylori-infected Mongolian Gerbils. Scand J Gastroenterol. 2003 Apr;38(4):361-369. doi: 10.1080/0036552031001699. PMID: 28240144.
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Scand J Gastroenterol. 2003 Apr;38(4):361-369. doi: 10.1080/0036552031001699.

Long-term Treatment with Sterigmatocystin, a Fungus Toxin, Enhances the Development of Intestinal Metaplasia of Gastric Mucosa in Helicobacter pylori-infected Mongolian Gerbils.

Scandinavian journal of gastroenterology

F Ma, J Misumi, W Zhao, K Aoki, M Kudo

Affiliations

  1. a Second Dept. of Public Health and Hygiene , Oita Medical University , Oita , Japan ; Dept. of Pharmacology , University of Tennessee Medical Center , Memphis , TN , USA.

PMID: 28240144 DOI: 10.1080/0036552031001699

Abstract

BACKGROUND: Helicobacter pylori is a human gastric carcinogen. Sterigmatocystin (ST), a fungus toxin, is a risk factor of gastric cancer. Cytotoxin-vacuolation toxin A (VacA) present in supernatants of H. pylori suspensions can cause gastritis and ulcer. The aim of this study was to examine the effects of H. pylori, ST and VacA in Mongolian gerbils.

METHODS: Male Mongolian gerbils (n = 196) were treated with H. pylori supernatants (10 ml/1000 mg) mixed with diet or inoculated intragastrically with H. pylori alone or with ST (100 or 1000 ppb), and then killed 27 months later. Gastric tissue sections were stained with haematoxylin and eosin (H&E), periodic acid-Schiff (PAS), Alcian blue (AB, pH 2.5) and with immunostaining for PCNA and p53 expression.

RESULTS: In H. pylori-infected gerbils, the normal mucosa was replaced by hyperplastic epithelium. Severe gastritis, cystic dilatation of gastric glands, hyperplastic polyps and intestinal metaplasia were observed. In H. pylori + ST (1000 ppb) gerbils, intestinal metaplasia was significantly more frequent than in H. pylori alone animals. 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 of the H. pylori + ST (1000 ppb) group were significantly higher than those of the other groups. PCNA labelling index and p53 index of infected gerbils were significantly higher than those of uninfected groups.

CONCLUSION: H. pylori causes gastritis, ulcer and intestinal metaplasia. ST enhances the development of intestinal metaplasia and increases gastrin levels in H. pylori-infected Mongolian gerbils.

Keywords: Gastrin level; Helicobacter pylori; Mongolian gerbils; intestinal metaplasia; osseous metaplasia; sterigmatocystin

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