弓形虫感染致早孕蜕膜自然杀伤细胞亚群的变化

Subset change of decidual NK cells infected by Toxoplasma gondii during early pregnancy

目的通过检测弓形虫感染后早孕蜕膜自然杀伤(NK)细胞亚群的变化,探讨其与弓形虫感染致不良妊娠结局的相关性。方法无菌获取10例正常健康早孕孕妇蜕膜组织,分离并纯化蜕膜NK细胞,培养24 h后平均分为2组:实验组细胞与弓形虫强毒株(RH株)共培养48 h,对照组加等量生理盐水。流式细胞分析实验组和对照组蜕膜NK细胞亚群的变化。结果实验组蜕膜NK细胞CD56+CD16-亚群所占比例为(48.83±21.99)%,对照组为(57.70±18.97)%;实验组CD56+CD16+亚群所占比例为(11.48±10.70)%,对照组为(4.45±4.24)%;实验组CD56+CD16-/CD56+CD16+比值为(10.92±17.84)%,对照组为(23.37±19.98)%;以上差异均有统计学意义(P<0.05)。实验组蜕膜NK细胞CD56+亚群所占比例为(60.31±22.53)%,对照组为(62.16±19.76)%,两组之间无统计学差异(P>0.05)。结论早孕期弓形虫感染可致蜕膜NK细胞CD56+CD16-亚群所占比例下降,且CD56+CD16+亚群所占比例上升,打破了正常妊娠时两者之间的平衡状态,这可能是早孕期弓形虫感染致不良妊娠结局的分子机制。

Objective To investigate the relationship between abnormal pregnancy and Toxoplasma gondii infection by examing the subset change of decidual natural killer （NK） cells infected by Toxoplasma gondii during early pregnancy. Methods Decidual tissues from 10 early human normal pregnant women were obtained after vaginal termination of pregnancy. Decidual NK cells were separated and purified with enzyme digestion, and divided equally into two groups after being incubated for 24 h. The experiment group was then co-cultured with Toxoplasma gondii for 48 h, while equal volume of normal saline was administed to the control group. The decidual NK cells were collected and cell subset change of the two groups was analyzed by flow cytometry. Results The CD56^＋ CD16^＋ subset accounted for （48.83 ±21.99）% of the decidual NK cells in the experiment group, and （57.70 ±18.97）% in the control group （P〈0.05）. That was （11.48 ±10.70）% in the experiment group and （4.45 ±4.24）% in the control group for CD56^＋CD16^＋ subset （ P〈 0.05）. The ratio ofCD56^＋ CD16^-/ CD56 ^＋CD16 ^＋was （10.92 ±17.84）% in the experiment group and （23.37 ±19.98）% in the control group （ P 〈 0.05）. The percentage of CD56 ^＋ decidual NK cells was （60.31 ± 22.53 ） % in the experiment group and （62.16 ±19.76） % in the control group （P 〉 0.05）. Conclusion During early pregnancy, Toxoplasma gondii infection could decrease the percentage of CD56^＋ CD16^- decidual NK cells and increase the percentage of CD56^＋ CD16^- subset, breaking the balance between CD56 ^＋ CD16^-and CD56^＋ CD16^- subset for the normal pregnancy. This molecular mechanism may play a role in human abnormal pregnancy infected by Toxoplasma gondii during early pregnancy.