Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-5-11
pubmed:abstractText
This study was to evaluate the levels of the proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha) and the cytokine inhibitors soluble TNF-alpha receptor (sTNFR) and interleukin (IL-1) receptor antagonist (IL-1ra), as well as the intensity of oxidative metabolism of peripheral blood polymorphonuclear leukocytes in the course of sepsis in newborns. An increase of TNF-alpha, sTNFR and IL-1ra concentrations was found in the blood serum of the patients at the time of diagnosis. This was further accompanied by polymorphonuclear leukocyte stimulation and, as a consequence of prolonged bacterial antigen stimulation, functional exhaustion of these cells and their diminished oxidative metabolism was observed. Within the same time period, an enhanced expression of p55 and p75 TNF-alpha receptors on polymorphonuclear leukocyte cell surfaces was found. It was indicated that the applied pharmacotherapy caused a decrease of the initially elevated concentrations of TNF-alpha and proinflammatory cytokine inhibitors (sTNFR, IL-1ra). The intensive therapy of sepsis was associated with the increased oxidative burst of polymorphonuclear leukocytes along with the decrease of p55 and p75 expression on their cell surfaces.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0004-069X
pubmed:author
pubmed:issnType
Print
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
155-61
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Proinflammatory cytokine inhibitors, TNF-alpha and oxidative burst of polymorphonuclear leukocytes in the pathogenesis of sepsis in newborns.
pubmed:affiliation
Department of Pediatric Propedeutics, Institute of Pediatrics, Medical University of Lód?, Poland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't