|
Sign In to gain access to subscriptions and/or personal tools.
|
Acute Parietal and Chief Cell Changes Induced by a Lethal Dose of Lipopolysaccharide in Mouse Stomach before Thrombus Formation
Kyoko Ito
Safety Research Laboratories, Yamanouchi Pharmaceutical Co Ltd, Tokyo, Japan,
Katsuhiko Ishida
Safety Research Laboratories, Yamanouchi Pharmaceutical Co Ltd, Tokyo, Japan
Takao Shishido
Safety Research Laboratories, Yamanouchi Pharmaceutical Co Ltd, Tokyo, Japan
Hajime Tabata
Safety Research Laboratories, Yamanouchi Pharmaceutical Co Ltd, Tokyo, Japan
Hisaki Miura
Safety Research Laboratories, Yamanouchi Pharmaceutical Co Ltd, Tokyo, Japan
Hideaki Okamiya
Safety Research Laboratories, Yamanouchi Pharmaceutical Co Ltd, Tokyo, Japan
Takanori Hanada
Safety Research Laboratories, Yamanouchi Pharmaceutical Co Ltd, Tokyo, Japan
The common lipopolysaccharide (LPS)-induced gastric lesions, such as erosions or ulcers, have been investigated in depth. Little is known, however, about the acute gastric lesions following a high dose of LPS. In a time-course study, ICR female mice were given a high subcutaneous dose of LPS (50 mg/kg). Mice were sacrificed at 4, 6, 12, and 24 hours after dosing and were assessed histopathologically for acute gastric lesions. The major gastric changes were seen in the fundic region and included vacuolar degeneration of parietal cells and apoptosis of chief cells. The vacuole in parietal cells was apparent as early as 4 hours postinjection (PI), and apoptosis of chief cells was apparent at 12 hours PI. Thrombus formation, in contrast, was not seen until 24 hours PI. No erosion, ulcer, or hemorrhage was seen in any gastric region in any of the treated animals at 24 hours PI. These results indicate that a subcutaneous high dose of LPS in mice causes vacuolar degeneration of parietal cells and apoptosis of chief cells before thrombus formation or subsequent ulcerative lesions.
Key Words: Lipopolysaccharide • gastric mucosa • acute • mice • vacuolation • parietal cell • apoptosis • chief cell
References
- Beales IL, Calam J. (1998). Interleukin-1 beta and tumor necrosis factor alpha inhibit acid secretion in cultured rabbit parietal cells by multiple pathways. Gut 42: 227-234.[Abstract/Free Full Text]
- Berczi I., Bertók L., Bereznai T. (1966). Comparative studies on the toxicity of Escherichia coli lipopolysaccharide endotoxin in various animal species. Can J Microbiol 12: 1070-1071.[Web of Science][Medline]
[Order article via Infotrieve]
- Berglindh T., Dibona DR, Ito S., Sachs G. (1980). Probes of parietal cell function. Am J Physiol 238: G165-G176.[Web of Science][Medline]
[Order article via Infotrieve]
- Bertman TA (1991). Mechanisms of gastrointestinal toxicity. In: Handbook of Toxicologic Pathology, Haschek WM, Rousseaux CG (eds). Academic Press, New York, pp 214-223.
- Fiorucci S., Santucci L., Migliorati G., Riccardi C., Amorosi A., Mancini A., Roberti R., Morelli A. (1996). Isolated guinea pig gastric chief cells express tumor necrosis factor receptors coupled with the sphingomyelin pathway. Gut 38: 182-189.[Abstract/Free Full Text]
- Hirata M. (1995). Pyrogenicity, vascular and coagulative systems and shock. In: Endotoxins, Nakano M, Kodama M (eds). Kodansha Scientific, Tokyo, pp 45-96.
- Karasawa H., Tani N., Miwa T. ( 1988). The effect of omeprazole on ultrastructural changes in gastric parietal cells. Gastroenterol Jpn 23: 1-8.[Medline]
[Order article via Infotrieve]
- Li J., Shimizu T. (1997). Course of apoptotic changes in the rat gastric mucosa caused by oral administration of Fusarenon-X. J Vet Med Sci 59: 191-199.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- Maeda Y. (1990). Study of acute gastric mucosal lesion induced by endotoxemia. Nippon Shokakibyo Gakkai Zasshi 78: 1-8.
- Mangeat P., Gusdinar T., Sahuquet A., Hanzel DK, Forte GF, Magous R. (1990). Acid secretion and membrane reorganization in single gastric parietal cell in primary culture. Biol Cell 69: 223-232.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- Mathan VI, Penny GR, Mathan MM, Rowley D. (1988). Bacterial lipopolysacccharide-induced intestinal microvascular lesions leading to acute diarrhea. J Clin Invest 82: 1714-1721.[Web of Science][Medline]
[Order article via Infotrieve]
- Mayeux PR (1997). Pathobiology of lipopolysaccharide. J Toxicol Environ Health 51: 415-435.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- Richardson RS, Norton LW, Sales Jel, Denver BE (1973). Gastric blood flow in endotoxin-induced stress ulcer. Arch Surg 106: 191-195.[Abstract/Free Full Text]
- Schultheis PJ, Clarke LL, Meneton P., Harline M., Boivin GP, Stemmermann G., Duffy JJ, Doetschman T., Miller ML, Shull GE (1998). Targeted disruption of the murine Na+/H+ exchanger isoform 2 gene causes reduced viability of gastric parietal cells and loss of net acid secretion. J Clin Invest 101: 1243-1253.[Web of Science][Medline]
[Order article via Infotrieve]
- Shiba T., Ikeda M., Hara A., Yoshida H., Kaneko H., Takeuchi S. (1990). Mechanism of acute gastrointestinal mucosal damage in endotoxic shock and the effect of fragmin. Semin Thromb Hemostasis 16(suppl): 55-59.[Web of Science][Medline]
[Order article via Infotrieve]
- Uehara A., Okumura T., Tsuji K., Taniguchi Y., Kitamori S., Takasugi Y., Namiki M. (1992). Evidence that gastric antisecretory action of lipopolysaccharide is not due to a toxic effect on gastric parietal cells. Dig Dis Sci 37: 1039-1044.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- Zherev S., Nikolov N. (1980). Gastric secretion of white rats in endotoxic shock. Probl Khig 8: 40-46.[Medline]
[Order article via Infotrieve]
Toxicologic Pathology, Vol. 28, No. 2,
304-309 (2000)
DOI: 10.1177/019262330002800210
 CiteULike  Complore  Connotea  Del.icio.us  Digg  Reddit  Technorati  Twitter What's this?
|
|
