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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2003-6-3
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pubmed:abstractText |
Helicobacter pylori induces symptomatic chronic gastritis in a subpopulation of infected individuals. The mechanism(s) determining the development and severity of pathology leading to symptoms are not fully understood. In a mouse model of H. pylori infection we analysed the influence of immunoregulatory CD4+CD25+ T cells on H. pylori colonization and gastritis. Athymic C57BL/6 nu/nu mice were reconstituted with (a) lymph node (LN) cells (b) LN cells depleted of CD25+ T cells (CD25(-) LN) or (c) not reconstituted at all. Mice were then infected orally with 3 x 10(8)H. pylori SS1 bacteria. At 2 and 6 weeks after the inoculation there was a significant (P < 0.001) reduction in H. pylori colonization in athymic mice transferred with CD25(-) LN cells compared to mice transferred with LN cells. Colonization was still reduced at 12 weeks after inoculation. Mice transferred with CD25(-) LN cells showed an earlier onset and increased severity of gastritis as compared to mice receiving LN cells. Splenic cells isolated from mice receiving CD25(-) LN cells produced the highest level of IFN-gamma on stimulation with H. pylori antigens in vitro, had a higher H. pylori-specific DTH response and increased infiltration of CD4+ T cells and macrophages in the gastric mucosa. Athymic mice not transferred with T cells had persistent high H. pylori colonization and displayed a normal gastric epithelium without inflammatory cells. In conclusion, CD4+CD25+ cells reduce immunopathology in H. pylori infection, possibly by reducing the activation of IFN-gamma producing CD4+ T cells, even at the expense of a higher H. pylori load in the gastric mucosa.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-10415051,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-10605010,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-10781854,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-10899916,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-11018139,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-11159999,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-11247637,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-11390498,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-11418648,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-11722621,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-11722634,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-11740498,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-11805149,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-11869680,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-11981815,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-12115645,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-12117975,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-12379718,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-12654789,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-2181029,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-7035348,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-7636184,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-9038313,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-9338786,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-9453604,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-9570536,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-9666600,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-9858514,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12780684-9864234
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0009-9104
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
132
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
393-400
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:12780684-Adoptive Transfer,
pubmed-meshheading:12780684-Animals,
pubmed-meshheading:12780684-CD4-Positive T-Lymphocytes,
pubmed-meshheading:12780684-Chronic Disease,
pubmed-meshheading:12780684-Disease Models, Animal,
pubmed-meshheading:12780684-Female,
pubmed-meshheading:12780684-Gastritis,
pubmed-meshheading:12780684-Helicobacter Infections,
pubmed-meshheading:12780684-Helicobacter pylori,
pubmed-meshheading:12780684-Immune Tolerance,
pubmed-meshheading:12780684-Immunity, Cellular,
pubmed-meshheading:12780684-Lymph Nodes,
pubmed-meshheading:12780684-Lymphocyte Activation,
pubmed-meshheading:12780684-Mice,
pubmed-meshheading:12780684-Mice, Inbred C57BL,
pubmed-meshheading:12780684-Mice, Nude,
pubmed-meshheading:12780684-Receptors, Interleukin-2,
pubmed-meshheading:12780684-T-Lymphocyte Subsets
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pubmed:year |
2003
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pubmed:articleTitle |
Absence of CD4+CD25+ regulatory T cells is associated with a loss of regulation leading to increased pathology in Helicobacter pylori-infected mice.
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pubmed:affiliation |
Department of Medical Microbiology and Immunology, Göteborg University, Göteborg, Sweden. sukanya.raghavan@microbio.gu.se
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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