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为探讨细胞间粘附分子-1(ICAM-1)参与脂多糖(LPS)刺激引起蜕膜细胞应激状态的机制,本研究采用LPS刺激和联合阻断ICAM-1及其受体LFA-1(CD11a/CD18,α1β1整合素)的策略,观察小鼠蜕膜LFA-1+细胞和调节性T细胞相对数量的改变,并检测胚胎吸收率的相应变化。LPS刺激可使小鼠胚胎丢失率显著增高,而采用中和抗体抑制ICAM-1/LFA-1通路则可基本消除这一效应。进一步研究发现,LPS可使小鼠蜕膜LFA-1+细胞相对数量显著增多,调节性T细胞相对数量显著减少。相反,抑制ICAM-1/LFA-1可消除上述LPS所造成的影响。结果提示,LPS刺激可激活ICAM-1/LFA-1信息通路,减少蜕膜Treg细胞的相对数量,并导致小鼠母-胎间免疫耐受失衡而发生流产。
In order to investigate the mechanism of ICAM-1 involved in the stress state of decidual cells induced by lipopolysaccharide (LPS) stimulation, LPS stimulation and combined blockade of ICAM-1 and its receptor LFA-1 (CD11a / CD18, α1β1 integrin) was used to observe the changes of the relative numbers of LFA-1 + cells and regulatory T cells in the decidua of mice and to detect the corresponding changes of the embryo absorption rate. LPS stimulation can significantly increase the rate of embryo loss in mice, while neutralizing antibody ICAM-1 / LFA-1 pathway can be basically eliminated this effect. Further study found that LPS can significantly increase the relative amount of LFA-1 + cells in mice, the relative number of regulatory T cells was significantly reduced. In contrast, inhibition of ICAM-1 / LFA-1 abolished the effects of LPS as described above. The results suggest that LPS stimulation can activate the ICAM-1 / LFA-1 signaling pathway, reduce the relative number of decidual Treg cells, and lead to imbalance in the mother-child immunocompromised abortion.