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首页> 外文期刊>Journal of Reproductive Immunology >Maternal environmental enrichment modulates the immune response against an inflammatory challenge during gestation and protects the offspring
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Maternal environmental enrichment modulates the immune response against an inflammatory challenge during gestation and protects the offspring

机译：母体环境富集在妊娠期间调节免疫应答，并保护后代

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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.
机译：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，暴露在丰富的环境（EE）中（EE被定义为对感觉通路的无创性和生物显著刺激，并结合自愿的体力活动）可以预防小鼠全身施用细菌脂多糖（LPS）引起的PTB和围产期死亡。本研究旨在分析EE是否调节外周血和羊水（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，我们发现与对照组相比，暴露于EE的母亲房颤中IL-10水平更高，B细胞百分比更高。尽管LPS显著增加了两组房颤患者的IL-6水平，但与EE相比，对照环境（CE）暴露组的IL-6水平高出3.6倍。同样，两组中的IL-22水平都显著增加，但在EE组中增加了6.7倍。有趣的是，房颤患者的PGE2水平仅在EE-LPS治疗组升高，并且观察到IL-22和PGE2水平之间存在正相关。在哺乳期，EE阻止了LPS诱导的生理标志物的延迟，这些标志物被分析用于评估后代的发育。我们的结果表明，EE调节了全身性LPS给药保护后代的免疫反应。我们建议为孕妇设计一个类似EE的方案，旨在防止早产儿出现后遗症。

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