Source:http://linkedlifedata.com/resource/pubmed/id/12874241
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2003-7-22
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pubmed:abstractText |
We have previously presented evidence demonstrating that mice deficient in NF-kappaB subunits are susceptible to colitis induced by the pathogenic enterohepatic Helicobacter species, H. hepaticus. However, it has not been determined whether NF-kappaB is required within inhibitory lymphocyte populations, within cells of the innate immune system, or both, to suppress inflammation. To examine these issues, we have performed a series of adoptive transfer experiments using recombination-activating gene (Rag)-2(-/-) or p50(-/-)p65(+/-)Rag-2(-/-) mice as hosts for wild-type (WT) and p50(-/-)p65(+/-) lymphocyte populations. We have shown that although the ability of H. hepaticus to induce colitis in Rag-2(-/-) mice is inhibited by the presence of either WT or p50(-/-)p65(+/-) splenocytes, these splenocyte populations are unable to suppress H. hepaticus-induced colitis in p50(-/-)p65(+/-)Rag-2(-/-) mice. Colitis in these animals is characterized by increased expression of inflammatory cytokines including IL-12 p40, and depletion of IL-12 p40 from p50(-/-)p65(+/-) mice ameliorates H. hepaticus-induced disease. Consistent with a primary defect in the regulation of IL-12 expression, H. hepaticus induced markedly higher levels of IL-12 p40 in p50(-/-)p65(+/-) macrophages than in WT macrophages. These results suggest that inhibition of H. hepaticus-induced IL-12 p40 expression by NF-kappaB subunits is critical to preventing colonic inflammation in response to inflammatory microflora.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Immune Sera,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12 Subunit p40,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Subunits,
http://linkedlifedata.com/resource/pubmed/chemical/Rag2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/V(D)J recombination activating...
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
171
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1484-92
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:12874241-Adoptive Transfer,
pubmed-meshheading:12874241-Animals,
pubmed-meshheading:12874241-Bone Marrow Cells,
pubmed-meshheading:12874241-Colitis,
pubmed-meshheading:12874241-DNA-Binding Proteins,
pubmed-meshheading:12874241-Helicobacter,
pubmed-meshheading:12874241-Immune Sera,
pubmed-meshheading:12874241-Immunity, Innate,
pubmed-meshheading:12874241-Injections, Intraperitoneal,
pubmed-meshheading:12874241-Interleukin-12,
pubmed-meshheading:12874241-Interleukin-12 Subunit p40,
pubmed-meshheading:12874241-Intestinal Mucosa,
pubmed-meshheading:12874241-Lymphocyte Subsets,
pubmed-meshheading:12874241-Macrophages,
pubmed-meshheading:12874241-Mice,
pubmed-meshheading:12874241-Mice, Inbred C57BL,
pubmed-meshheading:12874241-Mice, Knockout,
pubmed-meshheading:12874241-NF-kappa B,
pubmed-meshheading:12874241-Protein Subunits,
pubmed-meshheading:12874241-Spleen,
pubmed-meshheading:12874241-Up-Regulation
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pubmed:year |
2003
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pubmed:articleTitle |
NF-kappa B is required within the innate immune system to inhibit microflora-induced colitis and expression of IL-12 p40.
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pubmed:affiliation |
Department of Pathology, Brigham and Women's Hospital, Boston, MA 02115, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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