Choriodecidual leukocytes display a unique gene expression signature in spontaneous labor at term

Arenas‐Hernandez, Marcia; Gomez‐Lopez, Nardhy; Garcia‐Flores, Valeria; Rangel‐Escareño, Claudia; Álvarez-Salas, Luis Marat; Martínez-Acuña, Natalia; Vázquez-Pérez, Joel Armando; Vega-Sánchez, Rodrigo

doi:10.1038/s41435-017-0010-z

Cited by 19 publications

(15 citation statements)

References 86 publications

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“…Compared to the circulating neutrophils, those found in the chorio-decidua under homeostatic conditions had a higher expression of genes mediating extracellular matrix organization, angiogenesis, cell migration, and regulation of apoptotic processes and lower expression of genes involved in the inflammatory pathways such as TLR signaling and type I interferon signaling pathways. These findings are in line with recent data showing striking differences between the transcriptome of choriodecidua and maternal circulating leukocytes (37). Although the results seem counter-intuitive to the generally held notion that tissue neutrophils are proinflammatory, placenta neutrophils can sub-serve homeostatic functions and several studies report regulatory functions for these neutrophils (38)(39)(40).…”

Section: Discussionsupporting

confidence: 87%

TNF-Signaling Modulates Neutrophil-Mediated Immunity at the Feto-Maternal Interface During LPS-Induced Intrauterine Inflammation

et al. 2020

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Accumulation of activated neutrophils at the feto-maternal interface is a defining hallmark of intrauterine inflammation (IUI) that might trigger an excessive immune response during pregnancy. Mechanisms responsible of this massive neutrophil recruitment are poorly investigated. We have previously showed that intraamniotic injection of LPS in rhesus macaques induced a neutrophil predominant inflammatory response similar to that seen in human IUI. Here, we demonstrate that anti-TNF antibody (Adalimumab) inhibited ∼80% of genes induced by LPS involved in inflammatory signaling and innate immunity in chorio-decidua neutrophils. Consistent with the gene expression data, TNF-blockade decreased LPS-induced neutrophil accumulation and activation at the feto-maternal interface. We also observed a reduction in IL-6 and other pro-inflammatory cytokines but not prostaglandins concentrations in the amniotic fluid. Moreover, TNF-blockade decreased mRNA expression of inflammatory cytokines in the chorio-decidua but not in the uterus, suggesting that inhibition of TNF-signaling decreased the inflammation in a tissue-specific manner within the uterine compartment. Taken together, our results demonstrate a predominant role for TNF-signaling in modulating the neutrophilic infiltration at the feto-maternal interface during IUI and suggest that blockade of TNF-signaling could be considered as a therapeutic approach for IUI, the major leading cause of preterm birth.

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Section: Discussionsupporting

confidence: 87%

TNF-Signaling Modulates Neutrophil-Mediated Immunity at the Feto-Maternal Interface During LPS-Induced Intrauterine Inflammation

et al. 2020

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“…Several distinct immune cells populate the normal maternalfetal interface with distinct homeostatic roles during normal pregnancy (111). Immune cells in the choriodecidua have distinct immunological profiles and functions compared to their counterparts in blood (112). However, the repertoire of immune cells changes during IUI and parturition (113) and will be reviewed below ( Table 2).…”

Section: Immune and Non-immune Cells At The Feto-maternal Interfacementioning

confidence: 99%

Immunobiology of Acute Chorioamnionitis

2020

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Acute chorioamnionitis is characterized by neutrophilic infiltration and inflammation at the maternal fetal interface. It is a relatively common complication of pregnancy and can have devastating consequences including preterm labor, maternal infections, fetal infection/inflammation, fetal lung, brain, and gastrointestinal tract injury. In this review, we will discuss current understanding of the pathogenesis, immunobiology, and mechanisms of this condition. Most commonly, acute chorioamnionitis is a result of ascending infection with relatively low-virulence organisms such as the Ureaplasma species. Furthermore, recent vaginal microbiome studies suggest that there is a link between vaginal dysbiosis, vaginal inflammation, and ascending infection. Although less common, microorganisms invading the maternal-fetal interface via hematogenous route (e.g., Zika virus, Cytomegalovirus, and Listeria) can cause placental villitis and severe fetal inflammation and injury. We will provide an overview of the knowledge gleaned from different animal models of acute chorioamnionitis and the role of different immune cells in different maternal-fetal compartments. Lastly, we will discuss how infectious agents can break the maternal tolerance of fetal allograft during pregnancy and highlight the novel future therapeutic approaches.

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“…Labor is considered a state of systemic [15‐19] and local [20‐31] physiological inflammation [32‐35]. The latter concept is supported by consistent evidence showing that labor is characterized by an increase in cellular and soluble inflammatory mediators in the cervix [32,36‐48], myometrium [37‐38,40,49‐52], chorioamniotic membranes [38,40,53‐59], and decidual tissues (i.e.…”

Section: Introductionmentioning

confidence: 99%

The effects of advanced maternal age on T-cell subsets at the maternal–fetal interface prior to term labor and in the offspring: a mouse study

Levenson

Romero

Garcia‐Flores

et al. 2020

Clinical and Experimental Immunology

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Summary Women who conceive at 35 years of age or older, commonly known as advanced maternal age, have a higher risk of facing parturition complications and their children have an increased risk of developing diseases later in life. However, the immunological mechanisms underlying these pathological processes have yet to be established. To fill this gap in knowledge, using a murine model and immunophenotyping, we determined the effect of advanced maternal age on the main cellular branch of adaptive immunity, T cells, at the maternal–fetal interface and in the offspring. We report that advanced maternal age impaired the process of labor at term, inducing dystocia and delaying the timing of delivery. Advanced maternal age diminished the number of specific proinflammatory T‐cell subsets [T helper type 1 (Th1): CD4+IFN‐γ+, CD8+IFN‐γ+ and Th9: CD4+IL‐9+], as well as CD4+ regulatory T cells (CD4+CD25+FoxP3+ T cells), at the maternal–fetal interface prior to term labor. Advanced maternal age also altered fetal growth and survival of the offspring in early life. In addition, infants born to advanced‐age mothers had alterations in the T‐cell repertoire but not in CD71+ erythroid cells (CD3−CD71+TER119+ cells). This study provides insight into the immune alterations observed at the maternal–fetal interface of advanced‐age mothers and their offspring.

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Choriodecidual leukocytes display a unique gene expression signature in spontaneous labor at term

Cited by 19 publications

References 86 publications

TNF-Signaling Modulates Neutrophil-Mediated Immunity at the Feto-Maternal Interface During LPS-Induced Intrauterine Inflammation

TNF-Signaling Modulates Neutrophil-Mediated Immunity at the Feto-Maternal Interface During LPS-Induced Intrauterine Inflammation

Immunobiology of Acute Chorioamnionitis

The effects of advanced maternal age on T-cell subsets at the maternal–fetal interface prior to term labor and in the offspring: a mouse study

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