THE mechanisms whereby intrauterine contraceptive devices (IUDs) exert their anti-fertility effects remains unestablished1. The involvement of prostaglandins (PGs) is being investigated2-5, although alternative mechanisms have been proposed (for example, phagocytic and other actions of macrophages6,7). Although the relative contributions of macrophages and PGs to the anti-fertility actions of IUDs remains uncertain, it is clear that introduction of the IUD into the endometrial cavity results in an infiltration by neutrophils and macrophages8 as well as increased PG levels in uterine venous blood in animals9,10. While investigating the role of mediators of chronic inflammation we have demonstrated that the macrophage is a potent source of PGE11, and since the macrophage is the predominant cell adhering to the IUD6 we have considered the possibility that such cells act as a source of PGs.
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