Partial Protection againstHelicobacter pyloriin the Absence of Mast Cells in Mice

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Abstract
The goal of this study is to evaluate the contribution of mast cells toHelicobacter pyloriimmunity in a model of vaccine-induced protection. Mast cell-deficientKitlSl/KitlSl-dand control mice were immunized withH. pylorisonicate plus cholera toxin and challenged withH. pylori, and the bacterial loads, inflammatory infiltrates, and cytokine responses were evaluated and compared at 1, 2, and 4 weeks postchallenge. In vitro stimulation assays were performed using bone marrow-derived mast cells, and recall assays were performed with spleen cells of immunized mast cell-deficient and wild-type mice. Bacterial clearance was observed by 2 weeks postchallenge in mast cell-deficient mice. The bacterial load was reduced by 4.0 log CFU in wild-type mice and by 1.5 log CFU in mast cell-deficient mice. Neutrophil numbers in the gastric mucosa of immuneKitlSl/KitlSl-dmice were lower than those for immune wild-type mice (P< 0.05). Levels of gastric interleukin-17 (IL-17) and tumor necrosis factor alpha (TNF-α) were also significantly lower in immuneKitlSl/KitlSl-dmice than in wild-type mice (P< 0.001). Immunized mast cell-deficient and wild-type mouse spleen cells produced IFN-γ and IL-17 in response toH. pyloriantigen stimulation. TNF-α and CXC chemokines were detected in mast cell supernatants after 24 h of stimulation withH. pyloriantigen. The results indicate that mast cells are not essential for but do contribute to vaccine-induced immunity and that mast cells contribute to neutrophil recruitment and inflammation in response toH. pylori.

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