Submitted on August 12, 2004
Accepted on January 18, 2005
Host Specific Differences in the Physiology of Acid Secretion Related to Prostaglandins May Play a Role in Gastric Inflammation and Injury
Ireneusz T. Padol1 and Richard H. Hunt1*
1 Intestinal Disease Research Programme, McMaster University, Hamilton, Ontario, Canada
* To whom correspondence should be addressed. E-mail: huntr{at}mcmaster.ca.
Immune mediators are involved in strain specific manifestations of Helicobacter pylori infection
and the type of immune response is associated with production of PGE2, which in turn influences
gastric acid secretion. Acid secretion plays a pivotal role, not only in the pattern of Helicobacter
pylori induced gastritis and its consequences but also in NSAID induced gastropathies. Mice and
their transgenic modifications are widely used in Helicobacter and eicosanoid research and we
aimed to study acid secretion in gastric gland preparations from the commonly used strains of
Balb/c and C57BL/6 mice, using [14C]-aminopyrine (AP) accumulation and pylorus ligation. We
found that PGE2 does not inhibit acid secretion in gastric glands obtained from C57BL/6 mice, in
contrast to the expected antisecretory effect of PGE2 observed in Balb/c mice. In Balb/c mice, the
effect of histamine and carbachol was reduced by PGE2, while in C57BL/6 mice dose response
curves to these secretagogues were not affected. EP3 receptors are not involved in acid secretion
in C57BL/6 mice and this is confirmed by significantly lower expression of mRNA for the EP3
receptor. These contrary findings are important to the interpretation of the antisecretory role of
eicosanoids in Balb/c and C57BL/6 mouse strains and the involvement of prostanoids in the
etiology of Helicobacter induced inflammation and in NSAID induced gastropathies. We
propose that the lack of antisecretory effect of PGE2 observed in C57BL/6 mice could reflect the
extent of Helicobacter induced inflammation and status of acid secretion in response to anti-inflammatory
drugs.
