This review summarizes the information available on the involvement of
prostaglandins in blastocyst implantation, and examines their interac
tions with three other inflammatory mediators, platelet-activating fac
tor (PAF), interleukin 1 (IL-1) and corticotrophin-releasing factor (C
RF), Essential elements of this information, consistent with the assum
ption that prostaglandins play an important role in implantation, appe
ar to be: (i) the burst of endometrial prostaglandin production, follo
wing the blastocyst signal(s) or an artificial stimulus; (ii) the main
localization of this production at the luminal epithelium and release
towards the stroma; and (iii) the presence at the stromal level of sp
ecific progesterone-dependent binding sites for prostaglandin E(2) In
addition, accumulated data indicate a paracrine interaction at the end
ometrial level between PAF and prostaglandin E(2), which could serve,
among others, to amplify the embryonic signal(s), Pro-inflammatory cyt
okines IL-1 alpha and IL-1 beta may also play a significant role in en
dometrial response via the modulation of prostaglandin E(2) production
, Prostaglandins and IL-1 induce the expression of CRF, which acts as
an autocrine/paracrine inflammatory regulator, CRF exhibits a strong v
asoactivity in skin tests, inducing a local increase of capillary perm
eability at a concentrations of 10(-10) M, Levels of CRF and its mRNA
were found to be higher in rat implantation sites compared with those
in the interimplantation regions, Stromal cells were found to be posit
ive for immunoreactive CRF at the implantation sites only, It is sugge
sted that CRF may be involved in the local increase of capillary perme
ability seen in implantation sites, and that its production by stromal
cells may be the consequence of a paracrine action of epithelial pros
taglandin, released under the effect of PAF and IL-1, derived from or
produced by blastocysts in endometrial cells.