Nem. Vandoorn et al., LOCAL CELLULAR IMMUNE-RESPONSE IN THE ACUTE-PHASE OF GASTRITIS IN MICE INDUCED CHEMICALLY AND BY HELICOBACTER-PYLORI, Journal of Medical Microbiology, 47(10), 1998, pp. 863-870
Gastritis was induced in mice by oral administration of acetic acid 5%
, a cagA positive Helicobacter pylori strain, or both. The induction o
f a mild gastritis by acetic acid before inoculation with H, pylori re
sulted in a slight but not significantly decreased colonisation rate.
To study the initial stage of inflammation, the presence of gastric ly
mphoid and non-lymphoid cells was studied by immunohistochemistry duri
ng the first 2 weeks after induction of gastritis, Treatment with acet
ic acid alone or in combination with H, pylori resulted in an increase
in the number of neutrophils in the mucosa and submucosa, without evi
dent epithelial damage, The influx of neutrophils was most prominent i
n the mice that received a combined treatment of acetic acid and H, py
lori. Macrophages were also increased in both acetic acid and acetic a
cid plus H, pylori-treated groups, although a different kinetic patter
n was present in these groups. In mice infected with H, pylori alone,
only a slight but not significant increase in neutrophils and macropha
ges was observed, The early presence of lymphoid aggregates in the gas
tric mucosa of mice in which colonisation was shown with H, pylori was
remarkable, This phenomenon was not seen in control mice, in mice tha
t received acetic acid alone or when colonisation was not shown. These
data suggest that gastritis induced by a chemical agent such as aceti
c acid occurs by a different mechanism than gastritis induced by H. py
lori and that the continued presence of H. pylori is required for loca
l lymphocyte activation.