The production of pro-inflammatory cytokines during inflammatory processes has been associated with preterm birth (PTB) and fetal injury in humans and mice. We previously demonstrated that exposition to an enriched environment (EE), defined as a noninvasive and biological significant stimulus of the sensory pathway combined with voluntary physical activity, prevented PTB and perinatal death induced by the systemic administration of bacterial lipopolysaccharide (LPS) in mice. This work aimed to analyze whether EE modulates the immune response to the inflammatory process induced by LPS in peripheral blood and the amniotic fluid (AF). We observed that EE modulated maternal white blood cell count and its response to LPS. Furthermore, we found higher levels of IL-10 and a higher percentage of B cells in AF from EE exposed mothers compared to controls. Albeit LPS significantly increased IL-6 levels in AF from both groups, it was 3.6 times higher in control environment (CE) exposed group when compared to EE. Similarly, levels of IL-22 were significantly increased by LPS in both groups, but it was 6.7 times higher in EE group. Interestingly, levels of PGE2 in AF were only increased in the EE-LPS treated group, and a positive correlation between IL-22 and PGE2 levels was observed. During lactation, EE prevented LPS-induced delay in physical landmarks analyzed to assess offspring development. Our results suggest that EE modulates the immune response to systemic LPS-administration protecting the offspring. We propose that an EE-like protocol could be designed for pregnant women aiming at preventing the sequelae present in premature children.

炎症过程中促炎细胞因子的产生与人类和小鼠的早产 (PTB) 和胎儿损伤有关。我们之前已经证明，暴露于丰富的环境 (EE)，定义为感官通路的非侵入性和生物学显着刺激，结合自愿的身体活动，可防止由系统性施用细菌脂多糖 (LPS) 引起的 PTB 和围产期死亡。这项工作旨在分析 EE 是否调节对外周血和羊水 (AF) 中 LPS 诱导的炎症过程的免疫反应。我们观察到 EE 调节母体白细胞计数及其对 LPS 的反应。此外，我们发现与对照相比，暴露于 EE 的母亲的 AF 中 IL-10 水平更高，B 细胞百分比更高。尽管 LPS 显着增加了两组 AF 中的 IL-6 水平，但与 EE 相比，对照环境 (CE) 暴露组的水平高 3.6 倍。同样，LPS 组的 IL-22 水平在两组中均显着增加，但在 EE 组中高 6.7 倍。有趣的是，AF 中 PGE2 的水平仅在 EE-LPS 治疗组中增加，并且观察到 IL-22 和 PGE2 水平之间存在正相关。在哺乳期间，EE 可防止 LPS 引起的物理标志延迟，用于评估后代发育。我们的结果表明，EE 调节对全身 LPS 给药的免疫反应，从而保护后代。我们建议可以为孕妇设计类似 EE 的协议，旨在防止早产儿出现后遗症。