LABOR-ASSOCIATED INCREASE IN INTERLEUKIN-1-ALPHA RELEASE IN-VITRO BY HUMAN GESTATIONAL TISSUES

Citation
N. Laham et al., LABOR-ASSOCIATED INCREASE IN INTERLEUKIN-1-ALPHA RELEASE IN-VITRO BY HUMAN GESTATIONAL TISSUES, Journal of Endocrinology, 150(3), 1996, pp. 515-522
Citations number
39
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
00220795
Volume
150
Issue
3
Year of publication
1996
Pages
515 - 522
Database
ISI
SICI code
0022-0795(1996)150:3<515:LIIIRI>2.0.ZU;2-5
Abstract
The aims of this study were to investigate the concentration and relea se of interleukin-1 alpha (IL-1 alpha) at the time of human term labou r, and to study the regulation of IL-1 alpha release from human gestat ional tissue explants by bacterial endotoxin. Immunoreactive IL-1 alph a concentrations in maternal plasma, amniotic fluid and conditioned me dia from human amniotic, choriodecidual and placental explants were qu antified before and after spontaneous term labour-onset and delivery. Furthermore, the effects of a bacterial endotoxin, Lipopolysaccharide (LPS), on the release of IL-1 alpha horn human gestational tissue expl ants over a time course of 24 h (n=3) and LPS concentrations ranging f rom 10-10(7) pg/ml (n=3) were investigated. IL-1 alpha concentrations in material plasma and amniotic fluid did not change significantly wit h spontaneous term labour-onset. III contrast, IL-1 alpha was released in detectable amounts from human amniotic and choriodecidual explants only in association with term labour-onset and delivery, Similarly, p lacental release of IL-1 alpha was increased significantly in explant cultures in association with term labour,onset and delivery, LPS incre ased IL-1 alpha. release significantly only front human placental expl ants from both term not-in-labour and term after-labour tissues. The d ata demonstrate differential regulation of IL-1 alpha. release from hu man gestational tissues in association with labour and LPS treatment a nd the observations support the hypothesis that the labour-associated increase in IL-1 alpha release hom the fetal membranes is independent of exposure to bacterial endotoxin.