title: Proinflammatory cytokine inhibitors, TNF-alpha and oxidative burst of polymorphonuclear leukocytes in the pathogenesis of sepsis in newborns.
abstract: 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.
authors.affiliation: Department of Pediatric Propedeutics, Institute of Pediatrics, Medical University of Lódź, Poland.
authors.forename: J P
authors.initials: JP
authors.lastname: Sikora
authors.forename: D
authors.initials: D
authors.lastname: Chlebna-Sokół
authors.forename: I
authors.initials: I
authors.lastname: Dabrowska
authors.forename: D
authors.initials: D
authors.lastname: Lipczyński
authors.forename: S
authors.initials: S
authors.lastname: Chrul
mesh_terms: D015703:Antigens, CD / Q000097:blood; D002462:Cell Membrane / Q000276:immunology / Q000378:metabolism; D016207:Cytokines / Q000037:antagonists & inhibitors* / Q000097:blood*; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D053590:Interleukin 1 Receptor Antagonist Protein; D009504:Neutrophils / Q000276:immunology* / Q000378:metabolism*; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D016897:Respiratory Burst; D018805:Sepsis / Q000097:blood* / Q000209:etiology* / Q000276:immunology; D012795:Sialoglycoproteins / Q000097:blood; D012995:Solubility; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D015703:Antigens, CD; D016207:Cytokines; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha