Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1992-4-3
pubmed:abstractText
Increased concentrations of the soluble form of the interleukin 2 receptor have been observed in the sera of Crohn's disease and ulcerative colitis patients. In this study we have observed the spontaneous release of soluble interleukin 2 receptor by unstimulated, isolated normal and inflammatory bowel disease colonic lamina propria mononuclear cells. Lamina propria mononuclear cells from Crohn's disease patients (median = 204 U/ml (interquartile range 126-396, n 17) secreted significantly (p less than 0.01) more soluble interleukin 2 receptor than normal controls (median = 124.5 U/ml (108-131), n 12). No statistically significant differences were seen between ulcerative colitis (median = 135 U/ml (92-196), n 20) and normal controls. Moreover, significantly (p less than 0.01) increased amounts of soluble interleukin 2 receptor were secreted by colonic diverticulitis lamina propria mononuclear cells (median = 259 U/ml (149-282), n 15) which were used as disease specificity controls. Time course experiments showed that the majority of soluble interleukin 2 receptor was released by isolated lamina propria mononuclear cells in the first six days of culture. Upon stimulation with pokeweed mitogen, Crohn's disease (median = 2258 U/ml (1435-3584), n 14), normal control (median = 2622 U/ml (2030-3180), n 14) and diverticulitis lamina propria mononuclear cells (median = 2745 U/ml (1733-3192), n 10) reached similar maximal soluble interleukin 2 receptor secretion levels, while ulcerative colitis lamina propria mononuclear cells secreted significantly (p less than 0.005) less soluble interleukin 2 receptor (median = 912 U/ml (494-1259), n 17). These results suggest that enhanced shedding/secretion of soluble interleukin 2 receptor by intestinal lymphocytes may account in part for increased serum soluble interleukin 2 receptor concentrations during chronic intestinal inflammatory reactions.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-1889695, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-2142114, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-2208797, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-2210449, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-2298368, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-2347912, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-2370014, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-2424974, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-2498391, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-2821110, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-2990780, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-3019203, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-3023487, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-3040543, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-3116143, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-323291, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-3802572, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-3918914, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-3930598, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-6090574, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-6228498, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-6427329, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-6787129, http://linkedlifedata.com/resource/pubmed/commentcorrection/1541420-7042543
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0017-5749
pubmed:author
pubmed:issnType
Print
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
236-41
pubmed:dateRevised
2010-9-7
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Increased in vitro release of soluble interleukin 2 receptor by colonic lamina propria mononuclear cells in inflammatory bowel disease.
pubmed:affiliation
University of Pennsylvania, Gastrointestinal Section, Philadelphia, PA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't