This study explored the effects of uterine inflammation on eggshell mineralization, ultrastructure and mechanical properties in laying hens modified by a lipopolysaccharide (LPS) challenge or dietary essential oil (EO) addition. In trial 1, a total of 72 Hy-line Brown layers at 36 wk of age were randomly assigned to 3 treatment groups (n = 8), where they were intravenously injected with phosphate buffered saline, LPS at 1 mg/kg body weight, or LPS 3 times at 24-h intervals. In trial 2, a total of 288 Hy-line Brown layers at 60 wk of age were randomly divided into 4 groups (n = 8), where they were fed basal diets supplemented with EO at 0, 50, 100 and 200 mg/kg for 12 wk. A uterine inflammation model was constructed with LPS treatment, indicated by the elevated expression of IL-1β and TNF-α (P < 0.05) and lymphocyte infiltration. Uterine inflammation caused remarkable decreases in eggshell thickness and mechanical properties with structure deteriorations (P < 0.05). Uterine inflammation stimulated the expression of matrix proteins ovotransferrin (TF) and ovalbumin (OVAL), while depressing the mRNA levels of calbindin-1 (CALB1) and osteopontin in uterine mucosa (P < 0.05). In contrast, EO addition alleviated uterine inflammation, evidenced by depressed levels of IL-1β and IL-6 (P < 0.05). There was a significant elevation in shell thickness and breaking strength following EO intervention (P < 0.05), and these effects were maximized at addition of 100 mg/kg. Further, EO improved shell ultrastructure including more early fusion, less type B mammillae, and increased effective thickness (P < 0.05). The alleviated inflammation decreased the expression of OVAL and TF, whereas ion transport genes like CALB1 and solute carrier family 26 member 9 were upregulated (P < 0.05). Our findings suggest that inflammatory status can impact uterine functions in calcium transport and the synthesis of matrix proteins especially such as OVAL and TF, which in turn modulates calcium precipitation and ultrastructure formation, thereby determining eggshell mechanical properties. These findings provide a novel insight into the uterine inflammation-mediated modifications of eggshell quality.

本研究探讨了子宫炎症对通过脂多糖 (LPS) 挑战或添加日粮精油 (EO) 改良的蛋鸡蛋壳矿化、超微结构和机械特性的影响。在试验 1 中，总共 72 只 36 周龄的海兰褐蛋鸡被随机分配到 3 个处理组（n  = 8），静脉注射磷酸盐缓冲盐水、1 mg/kg 体重的 LPS，或 LPS 3 次，间隔 24 小时。在试验 2 中，总共 288 只 60 周龄海兰褐蛋鸡被随机分为 4 组（n  = 8），饲喂添加 0、50、100 和 200 mg/kg EO 的基础日粮持续 12 周。通过 LPS 处理构建子宫炎症模型，IL-1β、TNF-α（P  < 0.05）和淋巴细胞浸润。子宫炎症导致蛋壳厚度和机械性能显着下降，结构恶化（P  < 0.05）。子宫炎症刺激基质蛋白卵转铁蛋白（ TF）和卵清蛋白（OVAL ）的表达，同时降低子宫粘膜钙结合蛋白-1（CALB1 ）和骨桥蛋白的mRNA水平（ P  < 0.05）。相反，添加 EO 可减轻子宫炎症， IL-1β和IL-6水平降低即可证明（P < 0.05）。EO 干预后，壳厚度和断裂强度显着升高（P  < 0.05），并且这些效果在添加 100 mg/kg 时达到最大。此外，EO 改善了壳的超微结构，包括更多的早期融合、更少的 B 型乳头和增加的有效厚度 ( P  < 0.05)。炎症减轻降低了OVAL和TF的表达，而离子转运基因如CALB1和溶质载体家族 26 成员 9 则上调（P < 0.05）。我们的研究结果表明，炎症状态会影响子宫的钙转运功能和基质蛋白的合成，尤其是 OVAL 和 TF，进而调节钙沉淀和超微结构形成，从而决定蛋壳的机械性能。这些发现为子宫炎症介导的蛋壳质量改变提供了新的见解。