Document Detail


Antenatal betamethasone changes cord blood monocyte responses to endotoxin in preterm lambs.
MedLine Citation:
PMID:  14973182     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Corticosteroids are routinely administered to women at risk for preterm delivery to induce fetal lung maturation. Antenatal corticosteroids have immunomodulatory effects on fetal immune cells that are poorly understood. We hypothesized that maternal betamethasone would alter in fetal monocytes both the initiation of inflammation in response to pro-inflammatory stimuli and the resolution of inflammation by phagocytosis of apoptotic neutrophils. Preterm lambs at 124 d gestation were delivered 15 h, 1 d, 2 d, or 7 d after 0.5 mg/kg maternal intramuscular betamethasone. Monocytes from cord blood were isolated and cultured and results were compared with monocytes from preterm lambs exposed to maternal saline or monocytes from adult sheep. Phagocytosis of Escherichia coli was not changed, however, phagocytosis of apoptotic neutrophils was low in fetal monocytes but increased after 7 d exposure to maternal betamethasone to the level found in adult monocytes. Hydrogen peroxide production after endotoxin stimulus was significantly reduced to 7.1 +/- 2.2 micromol at 5 h, 8.7 +/- 2.9 micromol at 24 h, and 4.1 +/- 1.9 micromol at 48 h versus 16.4 +/- 3.6 micromol in control animals; at 7 d, the hydrogen peroxide production increased to 74.3 +/- 19.7 micromol (p < 0.05, per 10(6) monocytes). IL-6 production was reduced at 15 h after maternal betamethasone but at no other time point. Maternal betamethasone initially suppressed several fetal monocyte functions, however, at 7 d, measurements of initiation and resolution of inflammation were increased to levels similar to monocytes from adult sheep. The time-dependent changes in maternal betamethasone modulation of the responses of fetal monocytes may influence immune function of the preterm lamb after delivery.
Authors:
Boris W Kramer; Machiko Ikegami; Timothy J M Moss; Ilias Nitsos; John P Newnham; Alan H Jobe
Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.     Date:  2004-02-18
Journal Detail:
Title:  Pediatric research     Volume:  55     ISSN:  0031-3998     ISO Abbreviation:  Pediatr. Res.     Publication Date:  2004 May 
Date Detail:
Created Date:  2004-04-21     Completed Date:  2004-11-08     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0100714     Medline TA:  Pediatr Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  764-8     Citation Subset:  IM    
Affiliation:
University Children's Hospital, 97080 Würzburg, Germany. kramer_b@kinderklinik.uni.wurgburg.de
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MeSH Terms
Descriptor/Qualifier:
Adrenal Cortex Hormones
Animals
Anti-Inflammatory Agents / pharmacology*
Apoptosis
Betamethasone / pharmacology*
Cells, Cultured
Endotoxins / metabolism*
Escherichia coli / metabolism
Female
Fetal Blood / drug effects*,  metabolism
Glucocorticoids / pharmacology
Hydrogen Peroxide / metabolism,  pharmacology
Inflammation
Interleukin-6 / metabolism
Leukocyte Count
Monocytes / drug effects*,  metabolism
Neutrophils / metabolism
Phagocytosis
Sheep
Sodium Chloride / metabolism
Time Factors
Grant Support
ID/Acronym/Agency:
HD-12714/HD/NICHD NIH HHS; HL-65397/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Adrenal Cortex Hormones; 0/Anti-Inflammatory Agents; 0/Endotoxins; 0/Glucocorticoids; 0/Interleukin-6; 378-44-9/Betamethasone; 7647-14-5/Sodium Chloride; 7722-84-1/Hydrogen Peroxide

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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