Senthamaraikannan Paranthaman, Presicce Pietro, Rueda Cesar M, Maneenil Gunlawadee, Schmidt Augusto F, Miller Lisa A, Waites Ken B, Jobe Alan H, Kallapur Suhas G, Chougnet Claire A
Perinatal Institute.
Division of Immunobiology, Cincinnati Children's Hospital Medical Center and the University of Cincinnati College of Medicine, Ohio.
J Infect Dis. 2016 Nov 15;214(10):1597-1604. doi: 10.1093/infdis/jiw408. Epub 2016 Sep 6.
Although Ureaplasma species are the most common organisms associated with prematurity, their effects on the maternal and fetal immune system remain poorly characterized.
Rhesus macaque dams at approximately 80% gestation were injected intra-amniotically with 10 colony-forming units of Ureaplasma parvum or saline (control). Fetuses were delivered surgically 3 or 7 days later. We performed comprehensive assessments of inflammation and immune effects in multiple fetal and maternal tissues.
Although U. parvum grew well in amniotic fluid, there was minimal chorioamnionitis. U. parvum colonized the fetal lung, but fetal systemic microbial invasion was limited. Fetal lung inflammation was mild, with elevations in CXCL8, tumor necrosis factor (TNF) α, and CCL2 levels in alveolar washes at day 7. Inflammation was not detected in the fetal brain. Significantly, U. parvum decreased regulatory T cells (Tregs) and activated interferon γ production in these Tregs in the fetus. It was detected in uterine tissue by day 7 and induced mild inflammation and increased expression of connexin 43, a gap junction protein involved with labor.
U. parvum colonized the amniotic fluid and caused uterine inflammation, but without overt chorioamnionitis. It caused mild fetal lung inflammation but had a more profound effect on the fetal immune system, decreasing Tregs and polarizing them toward a T-helper 1 phenotype.
虽然脲原体是与早产相关的最常见微生物，但其对母体和胎儿免疫系统的影响仍未得到充分描述。
将妊娠约80%的恒河猴母猴经羊膜腔内注射10个细小脲原体菌落形成单位或生理盐水（对照）。3或7天后通过手术取出胎儿。我们对多个胎儿和母体组织中的炎症和免疫效应进行了全面评估。
虽然细小脲原体在羊水中生长良好，但绒毛膜羊膜炎很轻微。细小脲原体定殖于胎儿肺部，但胎儿全身性微生物入侵有限。胎儿肺部炎症较轻，在第7天肺泡灌洗液中CXCL8、肿瘤坏死因子（TNF）α和CCL2水平升高。在胎儿大脑中未检测到炎症。值得注意的是，细小脲原体减少了胎儿体内的调节性T细胞（Tregs），并激活了这些Tregs中干扰素γ的产生。在第7天时在子宫组织中检测到该病原体，它诱导了轻度炎症，并增加了连接蛋白43的表达，连接蛋白43是一种与分娩有关的缝隙连接蛋白。
细小脲原体定殖于羊水并引起子宫炎症，但无明显的绒毛膜羊膜炎。它引起了轻度胎儿肺部炎症，但对胎儿免疫系统有更深远的影响，减少了Tregs并使其向辅助性T细胞1表型极化。
