Caldeira M O, McDonald K S, Martinez E S M, Moraes J G N, Ramos I Sellmer, Poock S E, Ortega M S, Lucy M C
Division of Animal Sciences, University of Missouri, Columbia, MO, 65211, USA.
Department of Animal and Dairy Sciences, University of Wisconsin-Madison, Madison, WI, USA.
Theriogenology. 2025 Jul 1;240:117413. doi: 10.1016/j.theriogenology.2025.117413. Epub 2025 Mar 29.
The hypothesis was that early postpartum uterine disease would reduce the developmental capacity of oocytes thus contributing to the reduced fertility of dairy cows with uterine disease. Dairy cows were diagnosed healthy or with metritis at 7-10 d postpartum. The reproductive tract was collected at approximately 1 mo (Exp. 1) or approximately 80 or 165 d (Exp. 2) postpartum for the collection of cumulus-oocyte complexes (COC). The COC were matured, co-incubated with sperm for fertilization, and cultured to the blastocyst stage (8 d) in vitro. For Exp.1, the disease diagnosis (healthy or metritis) did not affect the number of collected COC or the subsequent embryo development to the blastocyst stage. The presence of purulent material in the uterine lumen (endometritis) at time of oocyte collection, however, was associated with a reduced cleavage rate evaluated 3 d following fertilization. For Exp. 2, there was no effect of disease diagnosis (healthy or metritis) on the number of COC or their subsequent development. Reduced cleavage rates were observed in COC retrieved from cows slaughtered at 80 d postpartum, but not at 165 d postpartum, and this reduction was associated with a vaginal microbiome indicative of uterine disease at 4-5 wk postpartum. Regression analyses that included plasma haptoglobin or energy metabolite concentrations or uterine bacterial genera abundance did not explain a large percentage of the variation in oocyte development in vitro. We conclude that there is an effect of uterine disease at one month postpartum on the oocyte and its capacity for development (Exp. 1) and this effect may be present at 80 d postpartum (Exp. 2). In later postpartum cows (165 d postpartum; Exp. 2) there was no effect of uterine disease on in vitro oocyte development.
研究假设是产后早期子宫疾病会降低卵母细胞的发育能力,从而导致患子宫疾病的奶牛生育力下降。在产后7至10天对奶牛进行健康或患子宫内膜炎的诊断。在产后约1个月(实验1)或约80天或165天(实验2)采集生殖道,以收集卵丘-卵母细胞复合体(COC)。将COC进行体外成熟培养,与精子共同孵育以进行受精,并培养至囊胚阶段(8天)。对于实验1,疾病诊断(健康或子宫内膜炎)不影响收集到的COC数量或随后胚胎发育至囊胚阶段。然而,在采集卵母细胞时子宫腔内存在脓性物质(子宫内膜炎)与受精后3天评估的卵裂率降低有关。对于实验2,疾病诊断(健康或子宫内膜炎)对COC数量或其随后的发育没有影响。在产后80天屠宰的奶牛中采集的COC观察到卵裂率降低,但在产后165天屠宰的奶牛中未观察到,这种降低与产后4至5周指示子宫疾病的阴道微生物群有关。包括血浆触珠蛋白或能量代谢物浓度或子宫细菌属丰度的回归分析并不能解释体外卵母细胞发育变异的很大比例。我们得出结论,产后1个月时子宫疾病对卵母细胞及其发育能力有影响(实验1),并且这种影响可能在产后80天存在(实验2)。在产后较晚阶段的奶牛(产后165天;实验2)中,子宫疾病对体外卵母细胞发育没有影响。