Send to

Choose Destination
See comment in PubMed Commons below
Biol Reprod. 1997 Sep;57(3):616-20.

Interleukin-8 release from human gestational tissue explants: the effects of lipopolysaccharide and cytokines.

Author information

  • 1Perinatal Research Centre, Department of Perinatal Medicine, The Royal Women's Hospital, Carlton, Victoria, Australia.


Interleukin (IL)-8 is a chemotactic cytokine that has been implicated in the etiology of infection-induced and normal human labor. In particular, IL-8 has been implicated in the processes of cervical ripening and rupture of fetal membranes because of its role in neutrophil activation and release of cellular matrix remodeling enzymes. In this study, we tested the hypotheses that IL-8 is released locally in the intrauterine environment from human amnion, choriodecidua, and placenta, and that IL-8 release from these tissues is increased by bacterial endotoxin, lipopolysaccharides (LPS), and inflammatory cytokines. IL-8 was released from human amnion, choriodecidual, and placental explants, with choriodecidua demonstrating the most abundant release. IL-8 release was significantly (multiple analysis of variance, p < 0.05) increased by LPS in a time- and dose-dependent manner from both choriodecidual and placental explants, but not from amnion explants. In addition, IL-1alpha (0.28 nM) and tumor necrosis factor alpha (TNFalpha, 10 nM) significantly (Student's t-test, p < 0.05) increased IL-8 release from placental explants 2- to 3-fold. These studies establish that the amnion, choriodecidua, and placenta are a source of IL-8 and demonstrate tissue-specific and differential regulation of IL-8 release by LPS, IL-1alpha, and TNF-alpha. These data support a role for IL-8 in a cascade of inflammatory events initiated by an intrauterine infection and resulting in activation of the labor process.

[PubMed - indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire
    Loading ...
    Write to the Help Desk