Document Detail


Influence of labor on neonatal neutrophil apoptosis, and inflammatory activity.
MedLine Citation:
PMID:  17413861     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Neutrophil apoptosis is impaired in neonates, and this contributes to prolonged inflammation and tissue injury in infants after infection or trauma. In the present studies, we investigated whether labor generates mediators that further suppress apoptosis. We found that neutrophil apoptosis was reduced in neonates exposed to labor, when compared with infants delivered by cesarean section before labor. This was not due to alterations in caspase-3 or inhibitor of apoptosis protein-2 (IAP-2). In contrast, labor primed neutrophils to express tumor necrosis factor alpha (TNF-alpha), suggesting that proinflammatory mediators contribute to reduced apoptosis after labor. Eicosanoids generated via cyclooxygenase-2 (Cox-2) and lipoxygenase (Lox) also regulate neutrophil apoptosis. 15-Lox, which generates proapoptotic lipoxins, but not Cox-2, was greater in neutrophils before labor, relative to cells exposed to labor. Anti-inflammatory eicosanoids exert their effects in part via peroxisome proliferator-activated receptor gamma (PPAR-gamma). Expression of gelatinase-associated lipocalin and catalase, two markers of PPAR-gamma activity, were increased in neonatal neutrophils before labor, relative to cells exposed to labor. These findings suggest that the anti-inflammatory environment is maintained before labor, in part, by eicosanoids. Although increased neutrophil longevity after labor is important for host defense in the immediate newborn period, it may contribute to inflammatory or oxidative injury in susceptible infants.
Authors:
Barry Weinberger; Anna M Vetrano; Kirin Syed; Sowmya Murthy; Nazeeh Hanna; Jeffrey D Laskin; Debra L Laskin
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Pediatric research     Volume:  61     ISSN:  0031-3998     ISO Abbreviation:  Pediatr. Res.     Publication Date:  2007 May 
Date Detail:
Created Date:  2007-06-05     Completed Date:  2007-07-16     Revised Date:  2007-12-03    
Medline Journal Info:
Nlm Unique ID:  0100714     Medline TA:  Pediatr Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  572-7     Citation Subset:  IM    
Affiliation:
Department of Pediatrics/Neonatology, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, New Jersey 08903, USA. weinbebi@umdnj.edu
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MeSH Terms
Descriptor/Qualifier:
Antioxidants / metabolism
Apoptosis / physiology*
Eicosanoids / metabolism
Female
Fetal Blood / cytology
Humans
Infant, Newborn
Inflammation / immunology*
Labor, Obstetric
Neutrophils / cytology,  physiology*
Pregnancy
Tumor Necrosis Factor-alpha / metabolism
Grant Support
ID/Acronym/Agency:
CA100994/CA/NCI NIH HHS; ES004738/ES/NIEHS NIH HHS; ES005022/ES/NIEHS NIH HHS; GM034310/GM/NIGMS NIH HHS; HD042036/HD/NICHD NIH HHS; HL067708/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Eicosanoids; 0/Tumor Necrosis Factor-alpha

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


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