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Creado el : 26 Feb 2004
Alterado em : 01 Dec 2007

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Ficha bibliográfica (sin autores) :

Labor induces a maternal inflammatory response syndrome. American Journal of Obstetrics and Gynecology 2004;190(2):448-455.

Autores :

Molloy EJ, O’Neill AJ, Grantham JJ, et al.

Año de publicación :

2004

URL(s) :

http://www.sciencedirect.com/science?_ob=ArticleUR…

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Abstract (English)  :

OBJECTIVE : We studied the effect of labor on maternal neutrophil phenotype.
STUDY DESIGN : Neutrophil apoptosis with inflammatory cytokines and the expression of CD11b, CD34 and toll-like receptor 4 (TLR4) were assessed with flow cytometry in women at uncomplicated vaginal delivery (VD), and elective cesarean section (ElCS) without labor, emergency cesarean section with (EmCSL+) or without (EmCSL-) labor.
RESULTS : Spontaneous neutrophil apoptosis is delayed in maternal neutrophils after VD, EmCSL+ or EmCSL- versus ElCS. In all groups lipopolysaccharide delayed apoptosis and increased CD11b expression. Elevated TLR4 expression in ElCS was associated with lipopolysaccharide responsiveness. CD34 was diminished in VD, indicating increased cell maturity.
CONCLUSION : Normal labor primes the neutrophil and may enhance antibacterial function by inducing a mild maternal inflammatory response syndrome. Delayed neutrophil apoptosis may promote the neutrophilia seen in women after VD. We suggest that labor of any duration may be immunologically beneficial to the parturient.

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Cécile Loup — 26 Feb 2004