Linked Life Data

9337148

Source:http://linkedlifedata.com/resource/pubmed/id/9337148

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1997-11-5
pubmed:abstractText
Nitric oxide (NO) from constitutive NO synthase (NOS) has been postulated to be a homeostatic regulator of leukocyte-endothelial cell interactions. By contrast, the inducible NO synthase (iNOS) isoform has been invoked as a potential pathogenic enzyme in numerous inflammatory diseases. The objective of this study was to determine whether the iNOS isoform is also capable of functioning as a regulator of leukocyte recruitment. Mice received endotoxin (LPS, 30 microg/kg, i.v.); 2-4 h later, intravital microscopy was used to examine leukocyte rolling and adhesion in postcapillary venules of the cremaster muscle and the sinusoids and postsinusoidal venules of the hepatic microcirculation. Leukocyte recruitment into the lung was also examined. RT-PCR confirmed that this treatment induced iNOS mRNA expression in wild-type mice as early as 2 h after LPS treatment. Between 2 and 4 h after LPS administration, the number of rolling and adherent leukocytes in cremasteric postcapillary venules and of adherent cells in liver postsinusoidal venules of iNOS-deficient mice were significantly higher than in wild-type mice. Leukocyte accumulation in the lung (measured by myeloperoxidase assay) was also significantly elevated in iNOS-deficient animals. These effects could not be attributed to differences in systemic blood pressure, shear rates, circulating leukocyte numbers, or baseline levels of rolling and adhesion because these parameters were not different between the two groups. To establish whether the differences in leukocyte recruitment were related to the leukocytes per se, perfusion of iNOS+/+ or iNOS-/- septic blood over purified E-selectin (using parallel plate flow chambers) revealed much larger recruitment of iNOS-/- leukocytes. These results suggest that iNOS induced in response to LPS releases NO that is capable of reducing leukocyte accumulation by affecting leukocytes directly and raises the possibility that induction of iNOS is a homeostatic regulator for leukocyte recruitment.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0892-6638
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
955-64
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9337148-Analysis of Variance, pubmed-meshheading:9337148-Animals, pubmed-meshheading:9337148-Blood Pressure, pubmed-meshheading:9337148-Chemotaxis, Leukocyte, pubmed-meshheading:9337148-Endothelium, Vascular, pubmed-meshheading:9337148-Endotoxemia, pubmed-meshheading:9337148-Endotoxins, pubmed-meshheading:9337148-Enzyme Induction, pubmed-meshheading:9337148-L-Selectin, pubmed-meshheading:9337148-Leukocytes, pubmed-meshheading:9337148-Lipopolysaccharides, pubmed-meshheading:9337148-Liver, pubmed-meshheading:9337148-Lung, pubmed-meshheading:9337148-Mice, pubmed-meshheading:9337148-Mice, Knockout, pubmed-meshheading:9337148-Microcirculation, pubmed-meshheading:9337148-Muscle, Skeletal, pubmed-meshheading:9337148-Nitric Oxide Synthase, pubmed-meshheading:9337148-Peroxidase, pubmed-meshheading:9337148-Polymerase Chain Reaction, pubmed-meshheading:9337148-RNA, Messenger, pubmed-meshheading:9337148-Transcription, Genetic
pubmed:year
1997
pubmed:articleTitle
Inducible nitric oxide synthase-deficient mice have enhanced leukocyte-endothelium interactions in endotoxemia.
pubmed:affiliation
Health Sciences Centre, University of Calgary, Alberta, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't