Sperm are allogenic to the female genital tract; however, oviducts provide optimal conditions for
survival and capacitation of these non-self cells until fertilization.Recently, we showed that oviduct-conditioned
media and prostaglandinE2 (PGE2) suppress sperm phagocytosis by polymorphonuclearneutrophils
(PMNs) under physiological conditions. We hypothesized that
sperm binding to bovine oviduct epithelial cells (BOECs) could change the local innate immunity
via PGE2. As the first step to obtain basic information, sub-confluent BOEC monolayers were
co-cultured with swim-up sperm for 2 h. BOECs with viable bound sperm were cultured for an
additional 3, 6, 12, or 24 h. Then, we confirmedthe impact of the sperm-BOECbinding on both
BOECs and PMN gene expression. Immunohistochemistry revealed that BOECs strongly
express TGFB1 and IL10 in the oviduct. Sperm binding to BOECs in culture induced the antiinflammatorycytokines
(TGFB1 and IL10) and PGE2 production by BOECs. Exogenous PGE2 in vitro suppressed pro-inflammatorycytokine expression (TNF and IL1B) in BOECs. Moreover,pre-exposure of PMNs to BOEC-conditioned media suppressed the TNF expression, but the BOEC media co-cultured with sperm stimulated PMNs to express TGFB1 and IL10, with increasing PGE2 secretion. Of note, exogenous PGE2 led PMNs in vitro to decrease their TNF expression and increase anti-inflammatory cytokines expression. Our findings strongly suggest that BOECs provide an anti-inflammatoryenvironment under physiological conditions and the sperm-BOECbinding furtherstrengthens this milieu thus suppresses PMNs in the bovine oviduct. PGE2 is likely to drive this stable anti-inflammatoryenvironment in the oviduct.