Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2007-3-22
pubmed:abstractText
In this study we examined mechanisms that regulate T-helper lymphocyte 1 (Th1) commitment in Helicobacter pylori-infected human gastric mucosa. The levels of gamma interferon (IFN-gamma), interleukin-4 (IL-4), and IL-12 in total extracts of gastric biopsies taken from H. pylori-infected and uninfected patients were determined by an enzyme-linked immunosorbent assay. The levels of signal transducer and activator of transcription 4 (STAT4), STAT6, and T-box expressed in T cells (T-bet) in total proteins extracted from gastric biopsies were determined by Western blotting. Finally, the effect of a neutralizing IL-12 antibody on expression of Th1 transcription factors and the levels of IFN-gamma in organ cultures of H. pylori-infected biopsies was examined. Increased levels of IFN-gamma and IL-12 were found in gastric biopsy samples of H. pylori-infected patients compared to the levels in uninfected patients. In addition, H. pylori-infected biopsies exhibited high levels of expression of phosphorylated STAT4 and T-bet. Higher levels of IFN-gamma and expression of Th1 transcription factors were associated with greater infiltration of mononuclear cells in the gastric mucosa. By contrast, production of IL-4 and expression of phosphorylated STAT6 were not associated with the intensity of mononuclear cell infiltration. In ex vivo organ cultures of H. pylori-infected biopsies, neutralization of endogenous IL-12 down-regulated the expression of phosphorylated STAT4 and T-bet and reduced IFN-gamma production. Our data indicated that IL-12 contributes to the Th1 cell commitment in H. pylori-infected human gastric mucosa.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-10358170, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-10444264, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-11114383, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-11397944, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-11786644, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-12370372, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-12461566, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-12500979, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-15153495, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-16543949, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-7638186, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-7698689, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-7905508, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-7907633, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-7994020, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-8700208, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-8827022, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-8943050, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-8943379, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-8993017, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-9053967, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-9120387, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-9120388, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-9160750, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-9174613, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-9181473, http://linkedlifedata.com/resource/pubmed/commentcorrection/17220306-9743537
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0019-9567
pubmed:author
pubmed:issnType
Print
pubmed:volume
75
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1738-44
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed-meshheading:17220306-Adult, pubmed-meshheading:17220306-Aged, pubmed-meshheading:17220306-Antibodies, pubmed-meshheading:17220306-Biopsy, pubmed-meshheading:17220306-Blotting, Western, pubmed-meshheading:17220306-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:17220306-Female, pubmed-meshheading:17220306-Gastric Mucosa, pubmed-meshheading:17220306-Helicobacter Infections, pubmed-meshheading:17220306-Helicobacter pylori, pubmed-meshheading:17220306-Humans, pubmed-meshheading:17220306-Interferon-gamma, pubmed-meshheading:17220306-Interleukin-12, pubmed-meshheading:17220306-Interleukin-4, pubmed-meshheading:17220306-Male, pubmed-meshheading:17220306-Middle Aged, pubmed-meshheading:17220306-Organ Culture Techniques, pubmed-meshheading:17220306-STAT4 Transcription Factor, pubmed-meshheading:17220306-STAT6 Transcription Factor, pubmed-meshheading:17220306-Signal Transduction, pubmed-meshheading:17220306-T-Box Domain Proteins
pubmed:year
2007
pubmed:articleTitle
Interleukin-12 drives the Th1 signaling pathway in Helicobacter pylori-infected human gastric mucosa.
pubmed:affiliation
Dipartimento di Medicina Sperimentale e Clinica, Università di Catanzaro Magna Graecia, Campus Universitario di Germaneto, Viale Europa, 88100 Catanzaro, Italy.
pubmed:publicationType
Journal Article