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Intraperitoneal Immunization Led to T Cell Hyporesponsiveness to Helicobacter pylori Infection in Mice
Author(s) -
Watanabe Koichiro,
Murakami Kazunari,
Maeda Kosaku,
Fujioka Toshio,
Nasu Masaru,
Nishizono Akira
Publication year - 2002
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.2002.tb02718.x
Subject(s) - immunology , immunization , splenocyte , helicobacter pylori , t cell , biology , immune system , gastritis , inflammation , immunity , regulatory t cell , il 2 receptor , genetics
During Helicobacter pylori infection, T cell response is critical in the development of active gastritis and in protective immunity against infection. We studied gastric inflammation and T cell response in H. pylori ‐challenged mice following an intraperitoneal immunization, using whole H. pylori lysate (HpAg) in the absence of adjuvants. H. pylori ‐challenged mice without immunization developed moderate to severe gastric inflammation, and splenocytes from these mice produced Th1 polarizing cytokines in response to HpAg and Con A during the acute infection. On the other hand, immunized‐challenged mice (those inoculated with H. pylori following immunization) had little or no gastric inflammation despite persistent H. pylori colonization. Our immunization primed splenocytes to produce IL‐2, IFN‐γ, and IL‐4 in response to HpAg and Con A before infection. However, these cells became hyporesponsive to both stimulants immediately after live bacterial challenge in terms of the production of these cytokines, especially IL‐2 and IFN‐γ. CTLA‐4 has been documented to be a negative regulator of IL‐2 production and lymphoproliferation that induces peripheral tolerance and functions 24–72 hr after the initiation of T cell activation. Compared with challenged mice, T cells from immunized‐challenged mice showed higher levels of CTLA‐4 expression at 72 hr after oral challenge. These data suggested that our immunization inhibited the development of H. pylori ‐associated gastritis and induced T cell hyporesponsiveness to H. pylori infection, which might be mediated by the early induction of CTLA‐4 following challenge.