|  Help  |  About  |  Contact Us

Publication : Partial protection against Helicobacter pylori in the absence of mast cells in mice.

First Author  Ding H Year  2009
Journal  Infect Immun Volume  77
Issue  12 Pages  5543-50
PubMed ID  19822650 Mgi Jnum  J:155471
Mgi Id  MGI:4414588 Doi  10.1128/IAI.00532-09
Citation  Ding H, et al. (2009) Partial protection against Helicobacter pylori in the absence of mast cells in mice. Infect Immun 77(12):5543-50
abstractText  The goal of this study is to evaluate the contribution of mast cells to Helicobacter pylori immunity in a model of vaccine-induced protection. Mast cell-deficient Kitl(Sl)/Kitl(Sl-d) and control mice were immunized with H. pylori sonicate plus cholera toxin and challenged with H. 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 immune Kitl(Sl)/Kitl(Sl-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-alpha) were also significantly lower in immune Kitl(Sl)/Kitl(Sl-d) mice than in wild-type mice (P < 0.001). Immunized mast cell-deficient and wild-type mouse spleen cells produced IFN-gamma and IL-17 in response to H. pylori antigen stimulation. TNF-alpha and CXC chemokines were detected in mast cell supernatants after 24 h of stimulation with H. 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 to H. pylori.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

5 Bio Entities

Trail: Publication

0 Expression