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Antiequine Chorionic Gonadotropin (eCG) Antibodies Generated in Goats Treated with eCG for the Induction of Ovulation Modulate the Luteinizing Hormone and Follicle-Stimulating Hormone Bioactivities of eCG Differently

Laboratoire Mécanismes d’Action des Gonadotropines, Unité Mixte de Recherche 6073, Institut National de la Recherche Agronomique/Centre National de la Recherche Scientifique/Université de Tours, Station de Physiologie de la Reproduction des Mammifères Domestiques, 37380 Nouzilly, France

Address all correspondence and requests for reprints to: Dr. M. C. Maurel, Laboratoire Mécanismes d’Action des Gonadotropines, Unité Mixte de Recherche 6073, Institut National de la Recherche Agronomique/Centre National de la Recherche/Université de Tours, Station de Physiologie de la Reproduction des Mammifères Domestiques, 37380 Nouzilly, France. E-mail: maurel{at}tours.inra.fr.

In dairy goats, treatments associating a progestogen and the equine chorionic gonadotropin (eCG) are the easiest way to induce and synchronize estrus and ovulation and to permit artificial insemination (AI) and/or out of season breeding. From the first treatment, the injection of eCG induces, in some females, the production of anti-eCG antibodies (Abs) that will interfere with the effectiveness of subsequent treatments. These anti-eCG Abs delay the preovulatory LH surge and the ovulation time, leading to poor fertility of the treated females. In this study, by in vitro bioassays, we show that anti-eCG Abs can positively or negatively modulate the LH and/or FSH bioactivities of eCG. Moreover, the modulation level of eCG bioactivity does not depend on the anti-eCG Ab affinity for eCG, as shown by surface plasmon resonance technology. The specificity of anti-eCG Abs tested by competitive ELISA highlighted the importance of a glycan environment in the recognition mechanism, especially the sialic acids specific to eCG. The different effects of anti-eCG Abs on eCG bioactivities could be explained by two hypotheses. First, steric hindrance preventing the interaction of eCG with its receptors would explain the inhibitory effect of some anti-eCG Abs; second, a conformational change in eCG by anti-eCG Abs could induce inhibition or potentiation of eCG bioactivities. It is significant that these modulations of eCG bioactivities by anti-eCG Abs impact mainly on the FSH bioactivity of eCG, which is essential for ovarian stimulation and subsequent fertility after treatment and AI, and to a lesser extent on LH bioactivity.

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