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Tytuł pozycji:

A model to study antioxidant regulation of endotoxemia-modulated neonatal granulopoiesis and granulocyte apoptosis.

Tytuł:
A model to study antioxidant regulation of endotoxemia-modulated neonatal granulopoiesis and granulocyte apoptosis.
Autorzy:
Yang KD; Chang Gung Children's Hospital at Kaohsiung, Kaohsiung 833, Taiwan.
Chen MZ
Teng RJ
Yang MY
Liu HC
Chen RF
Hsu TY
Shaio MF
Źródło:
Pediatric research [Pediatr Res] 2000 Dec; Vol. 48 (6), pp. 829-34.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Publication: 2012- : New York : Nature Publishing Group
Original Publication: Basel ; New York : Karger.
MeSH Terms:
Apoptosis*/drug effects
Hematopoiesis*/drug effects
Acetylcysteine/*pharmacology
Antioxidants/*pharmacology
Endotoxemia/*blood
Granulocytes/*pathology
Tumor Necrosis Factor-alpha/*antagonists & inhibitors
Adult ; Cells, Cultured/drug effects ; DNA Fragmentation/drug effects ; Endotoxemia/immunology ; Endotoxemia/physiopathology ; Endotoxins/pharmacology ; Fetal Blood/cytology ; Fetal Blood/drug effects ; Granulocytes/drug effects ; Humans ; Infant, Newborn ; Interleukin-8/pharmacology ; Oxidative Stress ; Reactive Oxygen Species
Substance Nomenclature:
0 (Antioxidants)
0 (Endotoxins)
0 (Interleukin-8)
0 (Reactive Oxygen Species)
0 (Tumor Necrosis Factor-alpha)
WYQ7N0BPYC (Acetylcysteine)
Entry Date(s):
Date Created: 20001205 Date Completed: 20010215 Latest Revision: 20131121
Update Code:
20240104
DOI:
10.1203/00006450-200012000-00021
PMID:
11102554
Czasopismo naukowe
Neonates with septicemia tend to develop granulocytopenia, which may, in part, be due to septic mediators such as oxygen free radicals and tumor necrosis factor alpha (TNF-alpha). Granulocytopenia may be caused by a decrease in granulocyte growth and/or an increase in granulocyte destruction. In the present study, we investigated antioxidant regulation of endotoxin-modulated neonatal granulopoiesis and granulocyte apoptosis. Using human umbilical cord blood (HUCB), we found that simulating endotoxemia in vitro elicited significant superoxide production within a few minutes. Endotoxin exposure suppressed colony-forming unit-granulocyte and monocyte formation in a dose-dependent fashion. Addition of antioxidants such as N-acetyl-cysteine could reverse the endotoxin suppression of colony-forming unit-granulocyte and monocyte formation (13 +/- 5 versus 75 +/- 5 colony-forming units/mL). Spontaneous in vitro granulocyte apoptosis in 6 h, as reflected by phosphatidylserine expression on the cell surface, was higher in granulocytes from HUCB than in those from adult blood (10.8 +/- 1.0% versus 5.6 +/- 1.2%). The addition of endotoxin or IL-8 to the cells in the in vitro model did not promote granulocyte apoptosis, but TNF-alpha, a major mediator of the effects of endotoxin, significantly induced granulocyte apoptosis in HUCB (control versus TNF-alpha: 8.9 +/- 1.2% versus 35.9 +/- 2.9%). Addition of the antioxidant N-acetyl-cysteine effectively blocked TNF-alpha-induced granulocyte apoptosis as demonstrated by DNA fragmentation. Results from these studies indicate that oxygen radicals are directly involved in endotoxin suppression of granulopoiesis, and indirectly promote granulocyte apoptosis, presumably through TNF-alpha-mediated action. Thus, under certain conditions, modulation of oxygen radical production in the blood may benefit neonates with granulocytopenia.

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