Comparative studies in pigs have shown that porcine SP proteins influence sperm physiology.5 As such, HBPs play a major role during sperm transport33, FK866 cost while the heterodimer PSP-I/PSP-II maintains fertilizing capacity.40,74 This beneficial effect depends on the PSP-II moiety, active at doses as low as 0.75 mg/mL,39 concentrations present in the first spurts of the boar ejaculate. As listed elsewhere, porcine HBPs spermadhesins coat the sperm membrane during ejaculation, producing structural changes to the sperm plasma membrane

in relation to capacitation, ZP recognition and fertilization. AWN follows, for instance, the spermatozoa up to the ZP,34 perhaps because of their role in inhibiting

sperm capacitation,75,76 an effect that is lost when this protein is removed from the sperm surface.33 At the same time, such initial layer of proteins might provide an anchor for aggregated spermadhesins to further coat the sperm surface,77 further stabilizing the plasmalemma and preventing pre-mature acrosomal exocytosis. The heparin-binding AQN-3, the most prominent ZP-binding protein in boar spermatozoa, remains – for instance – attached to the sperm surface after capacitation (in vitro) and can only be recovered from the aggregating raft area of the apical ridge of the sperm head.78,79 The non-heparin-binding protein PSP-I prevents pre-mature capacitation and acrosome exocytosis.80 selleck kinase inhibitor Whether these proteins are also involved in the interaction

between spermatozoa and oviductal epithelium during sperm capacitation remains to be explored. Increasing evidence exist that SP proteins are able to interact with the vaginal, cervical and, particularly, the uterine epithelium to elicit a series of changes in the immune responsiveness of the female, apparently modulated by pro- and anti-inflammatory SP proteins.81 This is not surprising, because the ejaculate (spermatozoa mafosfamide and SP) is to be considered foreign by the female and thus prompt to rejection. Deposition of semen into the vagina or the uterine cavity elicits a massive invasion of PMNs towards the lumen, followed by the formation of neutrophil extracellular traps (NETs) and sperm phagocytosis. Although PMN presence and infiltration are oestrogen-dependent,82 PMN migration to the surface epithelium and lumen can be elicited by SP glycoproteins (spermadhesins7) and pro-inflammatory-soluble cytokines83 (Fig. 2). This primary inflammatory reaction cleanses the intrauterine lumen from foreign cells, proteins and eventual pathogens, in preparation for the descending embryo. On the other hand, it does not occur in the oviduct, where spermatozoa find a haven until fertilization.8,9,27 Induction of PMN invasion is, evidently, not the only effect of the SP on the female.