Immune regulation by activation markers at feto-maternal interface in infection-associated spontaneous preterm birth

Abstract

BackgroundSpontaneous 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. AimTo 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. MethodsPlacental 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. ResultsThe 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. ConclusionsCD66a, 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.