Increased human leukocyte antigen-G expression at the maternal–fetal interface is associated with preterm birth

Stout, Molly J.; Cao, Bin; Landeau, Michele; French, J. I.; Macones, George A.; Mysorekar, Indira U.

doi:10.3109/14767058.2014.921152

Cited by 14 publications

(17 citation statements)

References 37 publications

(29 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Samples (5–8 mm) from the basal plate, chorionic villi, and amniotic membranes were obtained from placentas immediately after delivery. Tissues were processed as previously described (37). …”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

ATG16L1 governs placental infection risk and preterm birth in mice and women

Cao¹,

Macones²,

Mysorekar

2016

JCI Insight

Self Cite

View full text Add to dashboard Cite

The placenta is a barrier against maternal-fetal transmission of pathogens. Placental infections can cause several adverse pregnancy outcomes, including preterm birth (PTB). Yet, we have limited knowledge regarding the mechanisms the placenta uses to control infections. Here, we show that autophagy, a cellular recycling pathway important for host defense against pathogens, and the autophagy gene Atg16L1 play a key role in placental defense and are negatively associated with PTB in pregnant women. First, we demonstrate that placentas from women who delivered preterm exhibit reduced autophagy activity and are associated with higher infection indicators. Second, we identify the cellular location of the autophagy activity as being in syncytial trophoblasts. Third, we demonstrate that higher levels of autophagy and ATG16L1 in human trophoblasts were associated with increased resistance to infection. Accordingly, loss of autophagy or ATG16L1 impaired trophoblast antibacterial defenses. Fourth, we show that Atg16l1-deficient mice gave birth prematurely upon an inflammatory stimulus and their placentas were significantly less able to withstand infection. Finally, global induction of autophagy in both mouse placentas and human trophoblasts increased infection resistance. Our study has significant implications for understanding the etiology of placental infections and prematurity and developing strategies to mitigate placental infection–induced PTB.

show abstract

Section: Methodsmentioning

confidence: 99%

“…For histology, 5-mm sections were stained with Mayer’s Hematoxylin and Eosin Y solutions (Sigma-Aldrich). Immunohistochemistry was done as described previously (37). The following primary antibodies were used: anti-LC3 (1:200; Novus, NB600-1384), anti-P62 (1:500; Santa Cruz Biotechnology, SC28359), and anti-cytokeratin (1:1,000; DAKO, Z0622).…”

Section: Methodsmentioning

confidence: 99%

ATG16L1 governs placental infection risk and preterm birth in mice and women

Cao¹,

Macones²,

Mysorekar

2016

JCI Insight

Self Cite

View full text Add to dashboard Cite

show abstract

“…Whether this is true of commensal organisms has not yet been tested. Stout et al (19) recently found that placentas had an increase in HLA-G positivity in preterm births compared with those from term births, implying the contribution of maternal (host) factors in etiology of preterm birth. Whether and how changes in HLA-G levels affect the placental microbiome remains to be determined.…”

Section: Placenta the Microbiome And Preterm Birthmentioning

confidence: 99%

Placental Microbiome and Its Role in Preterm Birth

et al. 2014

Self Cite

View full text Add to dashboard Cite

Despite the well-known fact that the placenta has long-term effects on maternal and fetal health, the placenta remains a poorly understood and understudied organ. Not only is the placenta a site of exchange of nutrients and blood and gases between the fetal and maternal systems, but it also performs critical metabolic functions for supporting fetal development and maintaining maternal-fetal tolerance. It is also abundantly clear that impairment of placental function leads to severe pregnancy complications, including preterm birth (PTB), a significant cause of perinatal mortality and morbidity worldwide. Understanding the causes of PTB and other adverse outcomes is clearly essential for the development of effective methods of prevention and treatment. We focus our review of one major known cause of PTB, namely, infection. We also introduce a new and somewhat unexpected factor(s) that may well affect PTB and every aspect of placental biology and function: the placental microbiome. We discuss the implications of the placenta housing a microbial biomass for PTB and the effect of maternal microbiomes at various niches for fetal colonization and health outcomes. We suggest that the placenta is an integral part of the pipeline for microbe-powered driver of fetal destiny.

show abstract

“…A breakdown of maternal-fetal tolerance has been implicated in the mechanisms of disease responsible for a subset of recurrent pregnancy loss [10], fetal death [11,12], preterm labor [13][14][15][16][17][18], preterm prelabor rupture of the membranes (preterm PROM) [15] and other obstetrical complications [19][20][21][22][23][24].…”

Section: Introductionmentioning

confidence: 99%

Chronic inflammatory lesions of the placenta are associated with an up-regulation of amniotic fluid CXCR3: A marker of allograft rejection

Maymon

Romero

Bhatti

et al. 2018

Journal of Perinatal Medicine

View full text Add to dashboard Cite

Objective: The objective of this study is to determine whether the amniotic fluid (AF) concentration of soluble CXCR3 and its ligands CXCL9 and CXCL10 changes in patients whose placentas show evidence of chronic chorioamnionitis or other placental lesions consistent with maternal anti-fetal rejection. Methods: This retrospective case-control study included 425 women with (1) preterm delivery (n = 92); (2) term in labor (n = 68); and (3) term not in labor (n = 265). Amniotic fluid CXCR3, CXCL9 and CXCL10 concentrations were determined by ELISA. Results: (1) Amniotic fluid concentrations of CXCR3 and its ligands CXCL9 and CXCL10 are higher in patients with preterm labor and maternal anti-fetal rejection lesions than in those without these lesions [CXCR3: preterm labor and delivery with maternal anti-fetal rejection placental lesions (median, 17.24 ng/mL; IQR, 6.79-26.68) vs. preterm labor and delivery without these placental lesions (median 8.79 ng/mL; IQR, 4.98-14.7; P = 0.028)]; (2) patients with preterm labor and chronic chorioamnionitis had higher AF concentrations of CXCL9 and CXCL10, but not CXCR3, than those without this lesion [CXCR3: preterm labor with chronic chorioamnionitis (median, 17.02 ng/mL; IQR, 5.57-26.68) vs. preterm labor without chronic chorioamnionitis (median, 10.37 ng/mL; IQR 5.01-17.81; P = 0.283)]; (3) patients with preterm labor had a significantly higher AF concentration of CXCR3 than those in labor at term regardless of the presence or absence of placental lesions. Conclusion: Our findings support a role for maternal antifetal rejection in a subset of patients with preterm labor.

show abstract

Increased human leukocyte antigen-G expression at the maternal–fetal interface is associated with preterm birth

Cited by 14 publications

References 37 publications

ATG16L1 governs placental infection risk and preterm birth in mice and women

ATG16L1 governs placental infection risk and preterm birth in mice and women

Placental Microbiome and Its Role in Preterm Birth

Chronic inflammatory lesions of the placenta are associated with an up-regulation of amniotic fluid CXCR3: A marker of allograft rejection

Contact Info

Product

Resources

About