Kymioni Vasiliki M, Kakleas Konstantinos, Maria Lambropoulou, Sioga Antonia, Sarafidis Kosmas, Karachrysafi Sofia, Lialiaris Theodore, Papamitsou Theodora
Pediatrics, Agia Sofia Children's Hospital, Athens, GRC.
Allergy and Immunology, Agia Sofia Children's Hospital, Athens, GRC.
Cureus. 2024 Dec 23;16(12):e76246. doi: 10.7759/cureus.76246. eCollection 2024 Dec.
Maternal infections such as chorioamnionitis could impact fetal lung development by altering cell proliferation and apoptosis. Chorioamnionitis favors the multiple pleiotropic cytokines production such as LIF (leukemia inhibitory factor) and an inflammation-related protein p53. The cytokine production can lead to lung tissue damage and lung disease development.
The aim of the study is to evaluate the expression and the interaction of pro-anti-inflammatory proteins LIF and p53 on fetal lungs of all developmental stages after chorioamnionitis exposure.
Lung tissue was obtained from stillborn fetuses through elective abortion or miscarriage and was examined. This immuno-histochemical study aimed to evaluate the expression of pro-anti-inflammatory proteins LIF, and p53 on fetal lung tissues exposed to chorioamnionitis during three different stages of fetal lung development. Moreover, the interaction between LIF and p53 on inflammatory lung tissue was evaluated.
The comparison analysis of p53 rates in the three different stages showed that the p53 rate was significantly higher in the saccular stage compared to pseudogladular stage and canalicular stage, respectively (p-value: 0.05). The comparison analysis of LIF rates in the three different stages showed that the LIF rate was significantly higher in pseudogladular stage compared to the canalicular stage and saccular stage, respectively. No significant association between p53 and LIF was detected during the study duration period (p-value: 0.082).
The relationship between the two cytokines p53 and LIF interferes with the inflammation process. The result of their relation affects differently each stage of lung development as the cells maintain a different potential for differentiation and survival. Consequently, the extent of inflammation has a different importance at each stage.
绒毛膜羊膜炎等母体感染可通过改变细胞增殖和凋亡影响胎儿肺发育。绒毛膜羊膜炎有利于多种多效性细胞因子的产生，如白血病抑制因子（LIF）和一种炎症相关蛋白p53。细胞因子的产生可导致肺组织损伤和肺部疾病的发展。
本研究的目的是评估绒毛膜羊膜炎暴露后，促炎和抗炎蛋白LIF和p53在所有发育阶段胎儿肺中的表达及相互作用。
通过选择性流产或自然流产获取死产胎儿的肺组织并进行检查。这项免疫组织化学研究旨在评估促炎和抗炎蛋白LIF和p53在胎儿肺发育三个不同阶段暴露于绒毛膜羊膜炎的胎儿肺组织中的表达。此外，还评估了LIF和p53在炎性肺组织中的相互作用。
三个不同阶段p53率的比较分析表明，与假腺期和小管期相比，囊状期的p53率显著更高（p值：0.05）。三个不同阶段LIF率的比较分析表明，与小管期和囊状期相比，假腺期的LIF率显著更高。在研究期间未检测到p53与LIF之间存在显著关联（p值：0.082）。
两种细胞因子p53和LIF之间的关系干扰了炎症过程。它们关系的结果对肺发育的每个阶段有不同影响，因为细胞保持着不同的分化和存活潜能。因此，炎症程度在每个阶段具有不同的重要性。
