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Department of Clinical Immunology, Göteborg University, Göteborg, Sweden
We recently reported that Helicobacter pylori-specific Abs impair the development of gastritis and down-regulate resistance against H. pylori infection. In this study, we asked whether IgA Abs specifically can have an impact on H. pylori colonization and gastric inflammation. To obtain a sensitive model for the study of inflammation we crossed IgA- and IL-10-deficient mice. We found that IL-10–/–/IgA–/– mice were significantly less colonized than IL-10–/–/IgA+/+ mice, which in turn were less colonized than wild-type (WT) mice. The IL-10–/–/IgA–/– mice exhibited a 1.2-log reduction in bacterial counts compared with that in IL-10–/–/IgA+/+ mice, suggesting that IgA Abs rather promoted than prevented infection. The reduced colonization in IL-10–/–/IgA–/– mice was associated with the most severe gastritis observed, albeit all IL-10–/– mice demonstrated more severe gastric inflammation than wild-type mice. The gastritis score and the infiltration of CD4+ T cells into the gastric mucosa were significantly higher in IL-10–/–/IgA–/– mice than in IL-10–/–/IgA+/+ mice, arguing that IgA Abs counteracted inflammation. Moreover, following oral immunization, IL-10–/–/IgA–/– mice were significantly better protected against colonization than IL-10–/–/IgA+/+ mice. However, the stronger protection was associated with more severe postimmunization gastritis and gastric infiltration of CD4+ T cells. There was also a clear increase in complement receptor-expressing cells in IL-10–/–/IgA–/– mice, though C3b-fragment deposition in the gastric mucosa was comparable between the two. Finally, specific T cell responses to recall Ag demonstrated higher levels of IFN-
production in IL-10–/–/IgA–/– as compared with IL-10–/–/IgA+/+ mice. Thus, it appears that IgA and IL-10 help H. pylori bacteria evade host resistance against infection.
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