Changes in cervical interferon signaling at normal calving in dairy cows.

Cervical ripening promotes dilation of the birth canal and placental maturation facilitates the expulsion of fetal membranes after parturition, both of which involve coordinated inflammatory processes. Understanding the mechanisms that regulate sterile inflammation in uterine tissues is crucial for preventing periparturient complications in cattle, including dystocia, stillbirth, and retained placenta. Although we previously showed that attenuated upregulation of interferon (IFN) signaling in placentomes at calving is associated with retained placenta, the role of IFN signaling in sterile inflammation remains poorly understood. This study examined whether changes in IFN activity in the cervical mucosa during preparturition indicate inflammation during normal calving. Transcriptome analysis revealed increased expression of the IFN-stimulated genes ISG20 and IFIT1 at calving, similar to that observed in the placentomes. Real-time polymerase chain reaction revealed that IFNA, IFNG, and IFNT expression in the cervical mucosa decreased significantly at calving, whereas IFN-stimulated gene expression increased. Furthermore, ISG20 and MX2 levels showed highly consistent increases among individuals. Changes in IFN-related gene expression in peripheral blood leukocytes were less distinct than those in the cervical mucosa. Furthermore, IL1A, IL1B, IL8, and TNFA expression increased in the cervical mucosa, whereas IL6 expression decreased. Among these cytokine changes, IL1B and IL8 were consistent among individuals. These findings highlight IFN signaling as a common immune regulator in the cervix and placentomes at calving, indicating its potential utility in the development of predictive and preventive interventions for periparturient disorders associated with dysregulated sterile inflammation.