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Partial Protection againstHelicobacter pyloriin the Absence of Mast Cells in Mice
Author(s) -
Hua Ding,
John G. Nedrud,
Barry K. Wershil,
Raymond W. Redline,
Thomas G. Blanchard,
Steven J. Czinn
Publication year - 2009
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.00532-09
Subject(s) - biology , mast cell , immune system , immunology , cytokine , chemokine , spleen , tumor necrosis factor alpha , antigen , helicobacter pylori , histamine , microbiology and biotechnology , endocrinology , genetics
The goal of this study is to evaluate the contribution of mast cells toHelicobacter pylori immunity in a model of vaccine-induced protection. Mast cell-deficientKitlSl /KitlSl-d and control mice were immunized withH. pylori sonicate 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-d mice 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-d mice 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. pylori antigen stimulation. TNF-α and CXC chemokines were detected in mast cell supernatants after 24 h of stimulation withH. pylori antigen. 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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