N. Sawai et al., Role of gamma interferon in Helicobacter pylori-induced gastric inflammatory responses in a mouse model, INFEC IMMUN, 67(1), 1999, pp. 279-285
The immune responses to Helicobacter pylori infection play important roles
in gastroduodenal diseases. The contribution of gamma interferon (IFN-gamma
) to the immune responses, especially to the induction of gastric inflammat
ion and to protection from H. pylori infection, was investigated with IFN-g
amma gene knockout (IFN-gamma(-/-)) mice. We first examined the colonizing
abilities of eight H. pylori strains with a short-term infection test in or
der to select H, pylori strains which could colonize the mouse stomach. Onl
y three strains (ATCC 43504, CPY2052, and HPK127) colonized C57BL/6 wild-ty
pe mice, although all of the strains except for ATCC 51110 could colonize I
FN-gamma(-/-) mice. The number of H. pylori organisms colonizing the stomac
h in wild-type mice was lower than that in IFN-gamma(-/-) mice. Oral immuni
zation with the CPY2052 sonicate and cholera toxin protected against infect
ion with strain CPY2052 in both types of mouse. These findings suggested th
at IFN-gamma may play a protective role in H, pylori infection, although th
e degree of its protective ability was estimated to be low. In contrast, in
a long-term infection test done to examine the contribution of IFN-gamma t
o gastric inflammation, CPY2052-infected wild-type mice developed a severe
infiltration of mononuclear cells in the lamina propria and erosions in the
gastric epithelium 15 months after infection, whereas CPY2052-infected IFN
-gamma(-/-) mice showed no inflammatory symptoms. This result clearly demon
strated that IFN-gamma plays an important role in the induction of gastric
inflammation caused by H. pylori infection.