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Infection and Immunity, June 2001, p. 3891-3896, Vol. 69, No. 6
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.6.3891-3896.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Effect of Purified Lipopolysaccharides from Strains of Helicobacter pylori and Helicobacter felis on Acid Secretion in Mouse Gastric Glands In Vitro

Ireneusz T. Padol,1 Anthony P. Moran,2 and Richard H. Hunt1,*

Intestinal Disease Research Programme, McMaster University, Hamilton, Ontario, Canada,1 and Department of Microbiology, National University of Ireland, Galway, Ireland2

Received 28 November 2000/Returned for modification 22 January 2001/Accepted 13 March 2001

As a bacterial product, Helicobacter pylori lipopolysaccharide (LPS) can originate in close proximity to parietal cells, but the role of this uniquely structured endotoxin on acid secretion has not been fully investigated and remains unclear. The purpose of this study was to test the direct effect of purified LPS (tested range, 0.1 to 100 µg/ml) from various strains of H. pylori and from one Helicobacter felis strain on histamine- and carbachol-stimulated acid secretion in vitro using mouse gastric glands and the accumulation of [14C]aminopyrine. In addition, we investigated whether H. pylori LPS can interfere with two native antisecretory substances, prostaglandin E2 (PGE2) and somatostatin, which may contribute to bacterial pathogenicity. Except for the LPS from H. pylori SS1 (Sydney strain), which gave a statistically significant increase in both histamine- and carbachol-stimulated acid output (38 and 24%, respectively; P < 0.05), no effect of the tested LPS was observed on acid secretion. H. pylori LPS purified from a patient isolate did not affect the potency or the efficacy of the inhibitory dose response curve to PGE2 or somatostatin. Bacterial interstrain variation in the direct stimulatory effect of Helicobacter-derived LPS on acid secretion was observed, which probably reflects the molecular structure of LPS and the potential to contribute to virulence. Importantly, the data showed that H. pylori LPS did not have any direct antisecretory properties. It can be speculated that the acid stimulatory properties of LPS from H. pylori SS1 may contribute to the gastric damage observed in the mouse model of H. pylori infection.

* Corresponding author. Mailing address: McMaster University, Health Sciences Centre, Room 4W8, 1200 Main St. West, Hamilton, Ontario, L8N 3Z5, Canada. Phone: (905) 521-2100, ext. 76404. Fax: (905) 521-5072. E-mail: huntr{at}mcmaster.ca.

Infection and Immunity, June 2001, p. 3891-3896, Vol. 69, No. 6
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.6.3891-3896.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Padol, I T, Hunt, R H (2004). Effect of Th1 cytokines on acid secretion in pharmacologically characterised mouse gastric glands. Gut 53: 1075-1081 [Abstract] [Full Text]  


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