Bacterial infection of the amniotic cavity is one of the most frequent caus
es of preterm delivery. Bacterial products activate a network of autocrine
and paracrine mediators in fetal membranes and decidua, with prostaglandins
finally inducing contractions of the myometrium, Bradykinin and its B2-rec
eptor (B2R) seem to be part of this network. In cultured decidua-derived ce
lls, bradykinin stimulates the release of arachidonic acid, interleukin-6 (
IL-6), and interleukin-8 (IL-8), These effects are prevented by the specifi
c B2R antagonist Hoe 140, Using a pooled antiserum against peptide sequence
s of the B2R protein, the receptor can be visualized immunocytochemically,
The cells contain mRNA for the B2R, as shown by reverse transcriptase polym
erase chain reaction (RT-PCR). Binding studies reveal specific and saturabl
e binding sites for bradykinin with characteristics of the B2R, Binding of
bradykinin to the cells is enhanced by the inflammatory mediator interleuki
n-lp. In summary, human decidua-derived cells express the B2R, its expressi
on is upregulated in response to interleukin-lp, and bradykinin stimulates
the secretion of further mediators by these cells. Thus, bradykinin and the
B2R could play a central role in decidual activation. Lf so, B2R antagonis
ts would add to established tocolytic therapies that are applied together w
ith antibiotics in cases of chorioamnionitis at low gestational age.