Cell-free fetal DNA levels in maternal plasma after elective first-trimester termination of pregnancy

Wataganara, Tuangsit; Chen, Angela; LeShane, Erik S.; Sullivan, Lisa M.; Borgatta, Lynn; Bianchi, Diana W.; Johnson, Kirby L.

doi:10.1016/j.fertnstert.2003.07.028

Cited by 53 publications

(27 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This source of free fetal DNA is likely to arise from either destruction by the maternal immune system of fetal cells, which occasionally cross the placental barrier, or from placental and fetal cells that undergo apoptosis (16). Although normal pregnancies have a certain amount of fetal DNA present within the maternal circulation, this is quickly cleared after delivery (17).…”

mentioning

confidence: 99%

TLR9 Provokes Inflammation in Response to Fetal DNA: Mechanism for Fetal Loss in Preterm Birth and Preeclampsia

Scharfe-Nugent

Corr

Carpenter

et al. 2012

The Journal of Immunology

152

173

View full text Add to dashboard Cite

Preterm birth, the major cause of neonatal mortality in developed countries, is associated with intrauterine infections and inflammation, although the exact mechanisms underlying this event are unclear. In this study, we show that circulating fetal DNA, which is elevated in pregnancies complicated by preterm labor or preeclampsia, triggers an inflammatory reaction that results in spontaneous preterm birth. Fetal DNA activates NF-κB, shown by IκBα degradation in human PBMCs resulting in production of proinflammatory IL-6. We show that fetal resorption and preterm birth are rapidly induced in mice after i.p. injection of CpG or fetal DNA (300 μg/dam) on gestational day 10–14. In contrast, TLR9−/− mice were protected from these effects. Furthermore, this effect was blocked by oral administration of the TLR9 inhibitor chloroquine. Our data therefore provide a novel mechanism for preterm birth and preeclampsia, highlighting TLR9 as a potential therapeutic target for these common disorders of pregnancy.

show abstract

mentioning

confidence: 99%

TLR9 Provokes Inflammation in Response to Fetal DNA: Mechanism for Fetal Loss in Preterm Birth and Preeclampsia

Scharfe-Nugent

Corr

Carpenter

et al. 2012

The Journal of Immunology

152

173

View full text Add to dashboard Cite

show abstract

“…Only 50% of plasma samples from pregnant women with male fetus will be eligible for analysis Wataganara et al 19 Bisulphite sequencing…”

Section: Quantification Assay Target Of Measurement Details Referencesmentioning

confidence: 99%

Debates on fetal fraction measurement and DNA‐based noninvasive prenatal screening: time for standardisation?

Wataganara

et al. 2016

BJOG

View full text Add to dashboard Cite

“…The DAZ primers were the same as previously described. 32,33 The SRY primers amplify a single copy locus and along with the GAPDH positive control were described by Johnson et al 28 Both SYBR green (SABioscience and later Qiagen) and probe-based (SsoFast; BioRad) qPCR chemistry were used in several replicate reactions. Patients and family members were screened to determine the alleles inherited at a normal complement level.…”

Section: Detection Of Microchimeric Template Variationmentioning

confidence: 99%

Microchimerism and regulation in living related kidney transplant families

et al. 2014

View full text Add to dashboard Cite

Long-term harmful effects of immunosuppressive drugs and chronic rejection are a persistent impetus to establish methods to induce immunological tolerance to allografts. PCR-based studies have found evidence that humans and other placental mammals can have prolonged extremely low levels of maternal cells as well as other non-self cells, referred to as microchimerism. The persistence of these cells suggests a mechanism for the maintenance of the regulatory T-cell (Treg) responses frequently detected in offspring to non-inherited maternal antigens. We test the hypothesis that the detection of very low copy levels of insertion/deletion (Indel) alleles consistent with non-inherited maternal genes, will correlate with immune regulation to non-inherited maternal antigens as detected by a trans-vivo Delayed-Type Hypersensitivity (tvDTH) assay in kidney transplant recipients, normal donors and their immediate biological family members. Preliminary data reported here compares qPCR amplification of rare DNA templates in the peripheral blood polymorphonuclear (PMN) fraction of cells, with the results of tvDTH assays for linked suppression of recall antigen responses in the presence of non-inherited maternal antigens [NIMA]. The two assays do not show a definitive correlation.

show abstract

Cell-free fetal DNA levels in maternal plasma after elective first-trimester termination of pregnancy

Cited by 53 publications

References 24 publications

TLR9 Provokes Inflammation in Response to Fetal DNA: Mechanism for Fetal Loss in Preterm Birth and Preeclampsia

TLR9 Provokes Inflammation in Response to Fetal DNA: Mechanism for Fetal Loss in Preterm Birth and Preeclampsia

Debates on fetal fraction measurement and DNA‐based noninvasive prenatal screening: time for standardisation?

Microchimerism and regulation in living related kidney transplant families

Contact Info

Product

Resources

About