Impaired placentomal interferon signaling as the possible cause of retained fetal membrane in parturition-induced cows.

Although hormonal induction of parturition in cattle results in the successful delivery of healthy calves, the risk of retained fetal membrane is significantly increased. In a previous study, a combination of the long-acting glucocorticoid, triamcinolone acetonide, with a high dose of betamethasone partially normalized the placentomal gene expression during parturition; however, the incidence of retained fetal membrane remained high. This study further explored placentomal dysfunction and aimed to elucidate the mechanism of retained fetal membrane in parturition-induced cows. In this study, transcriptome analysis revealed that enhanced glucocorticoid exposure normalized the expression of a substantial fraction of genes in the cotyledons. In contrast, a significant reduction in the multiple signaling pathway activities, including interferon signaling, was found in the caruncles during induced parturition. Real-time PCR showed that the expression of interferon-tau in the caruncles, but not interferon-alpha or interferon-gamma, was significantly lower in induced parturition than spontaneous parturition. Interferon-stimulated gene expression was also significantly decreased in the caruncles during induced parturition. These results indicate that interferon signaling could be important for immunological control in placentomes during parturition. Additionally, this suggests that interferon-tau might be a pivotal ligand for interferon receptors in the caruncles. This study revealed that peripheral blood leukocytes in prepartum cows transcribed interferon-tau. Macrophage infiltration in the placentome is known to participate in the detachment of the fetal membrane from the caruncle. Thus, this study raised the possibility that immune cells migrating into the caruncles at parturition may act as a source of ligands that activate interferon signaling.

Expression of C-C motif chemokines and their receptors in bovine placentomes at spontaneous and induced parturition.

In bovine placentomes, the inflammatory response is considered important for the detachment of the fetal membrane from the caruncle after parturition. Glucocorticoids, a trigger of the onset of parturition, facilitate functional maturation of placentomes via prostaglandin (PG) and estrogen production in cattle. This study investigated how exogeneous glucocorticoids, which exert immunosuppressive effects, affect placental inflammation at parturition. Placentomes were collected immediately after spontaneous or induced parturition. Parturition was conventionally induced using PGF2α or dexamethasone or with a combination of triamcinolone acetonide and high-dose betamethasone (TABET treatment). Polymerase chain reaction (PCR) array analysis indicated that 9/13 C-C motif chemokine ligands (CCLs) were upregulated > two-fold in spontaneous parturition, with CCL2 and CCL8 being highly expressed. The expressions of CCL2, CCL8, C-C motif chemokine receptor 1 (CCR1), and CCR5 in caruncles were significantly higher in spontaneous parturition than in induced parturition. Although the clinical dose of dexamethasone did not influence the expression of these CCLs and CCRs, TABET treatment increased CCR1 expression. CCL8, CCR1, CCR2, and CCR5 were localized in the caruncular epithelial cells. CCR2 was also localized in the epithelial cells of the cotyledonary villi. This study is the first report to reveal the disruption in CCL and CCR expression in bovine placentomes at induced parturition. Enhanced glucocorticoid exposure for the induction of parturition may upregulate CCR1 expression in placentomes, but the treatment does not adequately promote CCL expression. Additionally, immunohistochemistry suggested that the CCL-CCR system is involved in the functional regulation of maternal and fetal epithelial cells in placentomes at parturition.

Metatranscriptomic Evidence for Magnetite Nanoparticle-Stimulated Acetoclastic Methanogenesis under Continuous Agitation.

Conductive nanomaterials have been reported to accelerate methanogenesis by promoting direct interspecies electron transfer (DIET), while their effects seem to vary depending on operational conditions. The present study examined the effects of magnetite nanoparticles (MNPs) on methanogenesis from acetate by soil-derived anaerobic cultures under continuous agitation. We found that MNPs accelerated methanogenesis in agitated cultures, as has been observed previously for static cultures. Metabarcoding of 16S rRNA gene amplicons showed that Methanosarcina substantially increased in the presence of MNPs, while DIET-related Geobacter did not occur. Metagenomic and metatranscriptomic analyses confirmed the predominance of Methanosarcina in MNP-supplemented agitated cultures. In addition, genes coding for acetoclastic methanogenesis, but not those for hydrogenotrophic methanogenesis, were abundantly expressed in the dominant Methanosarcina in the presence of MNPs. These results suggest that MNPs stimulate acetoclastic methanogenesis under continuous agitation.IMPORTANCE Previous studies have shown that conductive nanoparticles, such as MNPs, accelerate methanogenesis and suggested that MNPs facilitate DIET between exoelectrogenic bacteria and methanogenic archaea. In these methanogens, electrons thus obtained are considered to be used for hydrogenotrophic methanogenesis. However, the present work provides evidence that shows that MNPs accelerate DIET-independent acetoclastic methanogenesis under continuous agitation. Since most of previous studies have examined effects of MNPs in static or weakly agitated methanogenic cultures, results obtained in the present work suggest that hydraulic conditions definitively determine how MNPs accelerate methanogenesis. In addition, the knowledge obtained in this study is useful for engineers operating stirred-tank anaerobic digesters, since we show that MNPs accelerate methanogenesis under continuous agitation.