Passive immunization against progesterone inhibits endometrial sensitization in pseudopregnant mice and has antifertility effects in pregnant mice which are reversible by steroid treatment

Abstract

Pregnant mice were injected 32 h post coitum (p.c.) with a monoclonal antibody against progesterone (5·7 or 9·5 nmol immunoglobulin G (IgG)) or 0·9% (w/v) NaCl (controls). Progesterone was injected starting on day 2, 3, 4 or 5 p.c. Progesterone reversed the antifertility effect of the lower dose of antibody when replacement began on day 2, 3 or 4, though the number of implantation sites was reduced when treatment started on day 3 or 4. By day 5 only one of six treated animals remained pregnant, showing that antibody action was reversible only up to day 4. At the higher dose of antibody, exogenous nidatory oestrogen was also required. Pseudopregnant mice were injected 32 h p.c. with this antibody (5·7 nmol IgG) or 0·9% NaCl (controls). At 16.00 h on day 4 p.c., oil was injected into the lumen of one uterine horn and the magnitude of the decidual cell reaction was assessed 72 h later. Injected horns of antibody-treated females did not respond to intraluminal oil, whereas those of control mice increased fivefold in weight. Steroid treatment after the induction stimulus did not promote decidual growth, indicating that passive immunization reduced endometrial sensitivity. The results show that in the event that antibody fails to arrest the development of all embryos, the absence of endometrial sensitization will preclude the initiation of implantation, unless progesterone is given within 48 h of antibody treatment. J. Endocr. (1985) 104, 153–158