Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2005-5-30
pubmed:abstractText
Elevated soluble intercellular adhesion molecule-1 (sICAM-1) levels have been found in many pathological conditions, including obesity. To determine the effects of elevated sICAM-1 on immune responses and metabolism, we generated a transgenic mouse model overexpressing the extracellular domain of mouse ICAM-1 in the liver. The mice, showing 10-fold higher sICAM-1 levels than wild-type mice, presented elevated neutrophil count. Despite this, after intraperitoneal injection of thioglycollate, neutrophil recruitment into the peritoneal cavity was reduced, and the delayed macrophage recruitment was also affected in the transgenic mice compared with wild-type mice. Inhibition of contact hypersensitivity response in the sICAM-1 transgenic mice was comparable to ICAM-1-deficient mice and characterized by significantly less ear swelling and inflammatory cell infiltration than in wild-type mice. sICAM-1transgenic mice were more susceptible to weight gain on a Western-type diet than wild-type mice, and older animals showed excessive fat accumulation, again reminiscent of ICAM-1-deficient mice. Together, these data indicate that sICAM-1 interferes with ICAM-1-mediated cell-cell interactions, which could produce immune-suppressant effects and alteration of metabolism in persons with high levels of this soluble adhesion receptor.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1530-6860
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1018-20
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:15817637-Acquired Immunodeficiency Syndrome, pubmed-meshheading:15817637-Adiposity, pubmed-meshheading:15817637-Animals, pubmed-meshheading:15817637-DNA, pubmed-meshheading:15817637-Dermatitis, Contact, pubmed-meshheading:15817637-Dinitrofluorobenzene, pubmed-meshheading:15817637-Globins, pubmed-meshheading:15817637-Humans, pubmed-meshheading:15817637-Intercellular Adhesion Molecule-1, pubmed-meshheading:15817637-Introns, pubmed-meshheading:15817637-Liver, pubmed-meshheading:15817637-Macrophages, pubmed-meshheading:15817637-Mice, pubmed-meshheading:15817637-Mice, Inbred C57BL, pubmed-meshheading:15817637-Mice, Transgenic, pubmed-meshheading:15817637-Neutrophils, pubmed-meshheading:15817637-Peritonitis, pubmed-meshheading:15817637-Promoter Regions, Genetic, pubmed-meshheading:15817637-Solubility, pubmed-meshheading:15817637-Thioglycolates, pubmed-meshheading:15817637-alpha 1-Antitrypsin
pubmed:year
2005
pubmed:articleTitle
Elevated soluble ICAM-1 levels induce immune deficiency and increase adiposity in mice.
pubmed:affiliation
The CBR Institute for Biomedical Research, Harvard Medical School, Boston, Massachusetts 02115, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, N.I.H., Extramural