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Department of Veterinary Biosciences, Ohio State University, Columbus, OH 43210
Gastritis due to Helicobacter pylori in mice and
humans is considered a Th1-mediated disease, but the specific cell
subsets and cytokines involved are still not well understood. The goal
of this study was to investigate the immunopathogenesis of H.
pylori-induced gastritis and delayed-type hypersensitivity
(DTH) in mice. C57BL/6-Prkdcscid mice were
infected with H. pylori and reconstituted with
CD4+, CD4-depleted, CD4+CD45RBhigh,
or CD4+CD45RBlow splenocytes from wild-type
C57BL/6 mice or with splenocytes from
C57BL/6IFN-
-/- or
C57BL/6IL-10-/- mice. Four or eight weeks after transfer,
DTH to H. pylori Ags was determined by footpad
injection; gastritis and bacterial colonization were quantified; and
IFN- secretion by splenocytes in response to H.
pylori Ag was determined. Gastritis and DTH were present in
recipients of unfractionated splenocytes, CD4+ splenocytes,
and CD4+CD45RBhigh splenocytes, but absent in
the other groups. IFN- secretion in response to H.
pylori Ags was correlated with gastritis, although splenocytes
from all groups of mice secreted some IFN-. Gastritis was most
severe in recipients of splenocytes from IL-10-deficient mice, and
least severe in those given IFN--deficient splenocytes. Bacterial
colonization in all groups was inversely correlated with gastritis.
These data indicate that 1) CD4+ T cells are both necessary
and sufficient for gastritis and DTH due to H. pylori in
mice; 2) high expression of CD45RB is a marker for gastritis-inducing
CD4+ cells; and 3) IFN- contributes to gastritis and
IL-10 suppresses it, but IFN- secretion alone is not sufficient to
induce gastritis. The results support the assertion that H.
pylori is mediated by a Th1-biased cellular immune
response.
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