This review summarizes the information available on the involvement of prostaglandins in blastocyst implantation, and examines their interactions with three other inflammatory mediators, platelet-activating factor (PAF), interleukin (IL-1) and corticotrophin-releasing factor (CRF). Essential elements of this information, consistent with the assumption that prostaglandins play an important role in implantation, appear to be: (i) the burst of endometrial prostaglandin production, following 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 specific progesterone-dependent binding sites for prostaglandin E2. In addition, accumulated data indicate a paracrine interaction at the endometrial level between PAF and prostaglandin E2, which could serve, among others, to amplify the embryonic signal(s). Pro-inflammatory cytokines IL-1 alpha and IL-1 beta may also play a significant role in endometrial response via the modulation of prostaglandin E2 production. Prostaglandins and IL-1 induce the expression of CRF, which acts as an autocrine/paracrine inflammatory regulator. CRF exhibits a strong vasoactivity in skin tests, inducing a local increase of capillary permeability 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 positive for immunoreactive CRF at the implantation sites only. It is suggested that CRF may be involved in the local increase of capillary permeability seen in implantation sites, and that its production by stromal cells may be the consequence of a paracrine action of epithelial prostaglandin, released under the effect of PAF and IL-1, derived from or produced by blastocysts in endometrial cells.