背景:自发性早产(sPTB)是全球健康问题。研究表明,感染是sPTB的主要原因,免疫激活标记在sPTB期间调节母体针对病原体的免疫应答中起作用。
目的:研究活化标志物(CD66a,沙眼衣原体胎盘中的ICAM1,ITGB1,TIM3,CD25,CD95)和相关细胞因子(IL-1β和IL-17)/前列腺素受体(EP2和IP),人型支原体,解脲支原体感染的sPTB妇女。
方法:从160名sPTB和160名足月分娩妇女中收集胎盘样本。PCR用于沙眼衣原体的检测,人类M.解脲杆菌。激活标记物的mRNA表达,通过实时qPCR评估细胞因子和前列腺素受体。
结果:CD66a的倍数变化表达,ICAM1,TIM3,CD25和CD95分别为2.89,5.5,4.95,6.44和6.95倍(p<0.001),而细胞因子-IL-1β和IL-17分别为5.41和4.71倍(p<0.001),对于前列腺素受体,EP2和IP分别上调5.5和5倍(p<0.001),分别在感染sPTB的女性中。ICAM-1与IL-1β/EP2/IL-17、TIM3和IP/IL-17呈显著正相关。在感染sPTB的女性中,CD66a与EP2/IL-17,CD25与IL-1β/EP2,CD95与IL-1β/EP2之间存在显着负相关。
结论:CD66a,ICAM1和TIM3可能在炎症中起作用,并有可能在感染期间早产的临床开始,而CD25和CD95可能参与沙眼衣原体期间在生母界面的免疫耐受,人分枝杆菌和解脲支原体感染。
Spontaneous preterm birth (sPTB) is a global health concern. Studies reveal infections are majorly responsible for sPTB and immune activation markers play a role in regulation of maternal immune responses against pathogens during sPTB.
To study the mRNA expression and correlation of activation markers (CD66a, ICAM1, ITGB1, TIM3, CD25, CD95) and associated cytokines (IL-1β and IL-17)/prostaglandin receptors (EP2 and IP) in the placenta of Chlamydia trachomatis, Mycoplasma hominis, Ureaplasma urealyticum-infected sPTB women.
Placental samples were collected from 160 sPTB and 160 term birth women. PCR was used for the detection of C. trachomatis, M. hominis, U. urealyticum. The mRNA expression of activation markers, cytokines and prostaglandin receptors was evaluated by real-time qPCR.
The fold-change expression of CD66a, ICAM1, TIM3, CD25 and CD95 was 2.89, 5.5, 4.95, 6.44 and 6.95-fold (p < 0.001), respectively; while for cytokines- IL-1β and IL-17 was 5.41 and 4.71-fold (p < 0.001), respectively and for prostaglandin receptors- EP2 and IP was 5.5 and 5-fold (p < 0.001) upregulated, respectively in infected sPTB women. Significant positive correlation was obtained among ICAM-1 and IL-1β/EP2/IL-17, TIM3 and IP/IL-17. Significant negative correlation was obtained between CD66a and EP2/IL-17, CD25 and IL-1β/EP2, CD95 and IL-1β/EP2 in infected sPTB women.
CD66a, ICAM1 and TIM3 may play role in inflammation and have potential for the clinical beginning of preterm labour during infection while CD25 and CD95 are possibly involved in immunotolerance at feto-maternal interface during C. trachomatis, M. hominis and U. urealyticum infection.