Chorioamnionitis is an acute inflammatory
reaction associated with the premature rupture of the
fetal membranes. It is caused mainly by invasion of
bacteria from the vaginal tract that can penetrate the
intact membranes and invade the amnion cavity and the
decidua. Tight junctions (TJ) and adherent junctions
(AJ) are intercellular junctions crucial for epithelia
adhesion and permeability regulation in a wide variety of
tissues and organs. Our aim is to investigate if TJ and AJ
molecules are involved in human chorioamnionitis.
We studied the protein expression (by immunohistochemistry and western blotting) and the mRNA levels
(by RT-PCR) of some junction proteins such as Zonula
Occludens-1 (ZO-1), occludin, VE-cadherin and βcatenin in fetal membranes from women with
chorioamnionitis compared to those membranes derived
from idiopathic pregnancies.
Western blotting and immunohistochemical data
established that occludin expression was decreased in
amnion with chorioamnionitis compared to amnion from
idiopathic pregnancies. Samples tested for ZO-1, VEcadherin and β-catenin (proteins and mRNAs) showed
no differences between idiopathic and pathological
membranes.
One of the most relevant results is the decrease of
occludin in membranes with chorioamnionitis. Since we
have previously demonstrated that some cytokines,
particularly elevated in the chorioamnionitis, cause the
disruption of TJs in placental villi, we suggest that the
decrease of occludin in amnion may be the first change
that leads to the rupture of the amniotic membrane in
this pathology