Chorionic plate vessels as an origin of amniotic fluid neutrophils

Abstract

The present study was conducted to investigate the potential anatomical source of amniotic fluid neutrophils. Microdissection of neutrophils from the chorioamnion of the fetal membranes and the amnion of the chorionic plates of 10 preterm placentas with acute chorioamnionitis was performed and the genotypes of the neutrophils were compared with those of the mother and fetus using polymerase chain reaction of nine autosomal STR loci. In separate analyses, we reviewed eight cases of fetal autopsies with increased amniotic fluid neutrophils for the presence of neutrophils in the alveoli, and also analyzed the relationship between the amniotic fluid white blood cell (WBC) count and the histological pattern of placental inflammation. The genotypes of all of the neutrophils found in the chorioamnion of the fetal membrane matched those of the mother (n = 10). The genotypes of neutrophils found in the chorionic plate were of mixed maternal and fetal origin (n = 4). In the autopsy series of the fetuses with amniotic fluid WBC (n = 8), only five cases showed neutrophils in the alveolar space, while all the placentas had chorioamnionitis. There was no significant difference in amniotic fluid WBC count between the cases with or without acute membranitis, while among the cases with placental inflammation, those with inflammation of the chorionic plate had a significantly higher amniotic fluid WBC count than both the membranitis-only cases (P < 0.001) and the membranitis and funisitis cases (P < 0.05). These results imply that fetal vasculature at the chorionic plate is the main source of amniotic fluid neutrophils, especially in the cases without funisitis.

Are amniotic fluid neutrophils in women with intraamniotic infection and/or inflammation of fetal or maternal origin?

“…Indeed, a previous report implied that neutrophils migrate from the fetal vasculature of the chorionic plate (i.e. chorionic vasculitis) into the amniotic cavity 51 , particularly in those cases without acute umbilical phlebitis or arteritis.…”

“…Yet, experimental evidence showed that amniotic fluid neutrophils from women 49 or rhesus monkeys 50 undergoing preterm labor were of fetal origin. In such cases, these innate immune cells could originate from the fetal vessels of the chorionic plate 51 . However, abundant neutrophils have also been observed in the amniotic fluid of women with a severe maternal inflammatory response without a fetal inflammatory response in the placenta 13, 46 , indicating that further research is required to investigate whether, amniotic fluid neutrophils are of maternal origin or a mixture of both fetal and maternal neutrophils.…”

Lipopolysaccharide increases alveolar type II cell number in fetal mouse lungs through Toll-like receptor 4 and NF-κB

“…Cells within the placenta, amniotic membranes, and uterus can all participate in the innate immune response, secreting cytokines and chemokines including IL-8, IL-10, monocyte chemoattractant protein-1, and regulated on activation, normal T-expressed and presumably secreted (RANTES) (6,25). In addition, fetus-derived neutrophils can occupy the amniotic fluid in chorioamnionitis (18). Although we have shown the fetal lung can directly respond to endotoxin, the contribution of cells in the uterus, placenta, and amniotic membranes could alter how the fetal innate immune system responds to both microbial products and inflammatory mediators.…”

Neutrophil Extracellular Traps in the Amniotic Cavity of Women with Intra-Amniotic Infection: A New Mechanism of Host Defense

“…[39][40][41][42][43][44][45][46][47][48] Neutrophils are the most abundant leukocytes in the amniotic fluid in cases of intra-amniotic infection. 19 These innate immune cells seem to be fetal 49 and originate from the chorionic plate; 50 yet, further evidence is required to prove their fetal origin using genetic fingerprinting. Recently, using immunophenotyping, we demonstrated that amniotic fluid neutrophils express proinflammatory cytokines such as tumor necrosis factor-a, macrophage inflammatory protein (MIP)-1a, MIP-1b, interleukin (IL)-1a, IL-1b, and IL-8.…”