NOD1 and NOD2 control the invasiveness of trophoblast cells via the MAPK/p38 signaling pathway in human first-trimester pregnancy

Wang, Z.; Liu, M.; Nie, Xiaoqin; Zhang, Y.; Chen, Y.; Zhu, Liqiong; Chen, X.; Chen, L.; Chen, H.; Zhang, J.

doi:10.1016/j.placenta.2015.03.004

Cited by 31 publications

(19 citation statements)

References 39 publications

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“…31 Additional studies reported that p38MAPK signaling pathway controls the invasiveness of trophoblast cells in human first-trimester pregnancy. 32 In 2010, authors firstly investigated the human placental expression of p38MAPK in pregnancies complicated by HELLP and reported a significantly decreased expression of p38MAPK 33 (Fig. 1).…”

Section: Inflammationmentioning

confidence: 99%

Innate Immune System at the Maternal–Fetal Interface: Mechanisms of Disease and Targets of Therapy in Pregnancy Syndromes

Triggianese

Perricone

Chimenti

et al. 2016

American J Rep Immunol

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The maternal-fetal interface is an immunologically unique site that allows the tolerance to the allogenic fetus and maintains host defense against possible pathogens. Balanced immune responses are required for the maintenance of successful pregnancy. It has been demonstrated that innate immune disturbances may be responsible for some adverse pregnancy outcomes such as preeclampsia (PE); hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome; intrauterine growth restriction (IUGR); and recurrent spontaneous abortion (RSA). Observational studies suggest that immunomodulatory treatments in pregnancy-specific complications may improve both the hematological/biochemical features in the mother and the perinatal outcomes. The following review will discuss how recent and relevant findings in the field of the innate immunity have advanced our understanding of the role of inflammation and innate immune system in the pathogenesis of pregnancy failure and will discuss the therapeutic outcomes of the existing studies and clinical trials in light of these new insights.

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Section: Inflammationmentioning

confidence: 99%

Innate Immune System at the Maternal–Fetal Interface: Mechanisms of Disease and Targets of Therapy in Pregnancy Syndromes

Triggianese

Perricone

Chimenti

et al. 2016

American J Rep Immunol

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“…This differential expression is also observed functionally; the first trimester trophoblast cells trigger an inflammatory response following exposure to the NOD1 and NOD2 protein ligands, while trophoblast cells from term pregnancies only respond to the NOD1 ligand [94]. Interestingly, Wang et al demonstrated that expression of NOD1 and NOD 2 in placental villi and decidua was higher in epithelium than in tissue stroma, reinforcing the idea that epithelial tissues are strongly involved in the host defense response at the maternal-fetal interface [96].…”

Section: Tlrs and Nlrs At The Maternal-fetal Interface And Pregnancy mentioning

confidence: 84%

“…While several studies showed that gestational tissues express TLRs and are capable of responding to pathogens who present TLR-specific ligands, few studies have discussed the expression of NLRs at the maternal-fetal interface during normal and complicated pregnancies [92][93][94][95][96][97]. Gene expression of NOD1 was observed in the placenta of pregnant women at term [92,93], while first trimester placenta villi expressed NOD1 and NOD2 mRNA, both by syncytiotrophoblast and Spontaneous Prematurity, Innate Immune System, and Oxidative Stress at the Maternal-Fetal… DOI: http://dx.doi.org /10.5772/intechopen.88379 cytotrophoblast cells [94].…”

Section: Tlrs and Nlrs At The Maternal-fetal Interface And Pregnancy mentioning

confidence: 99%

Spontaneous Prematurity, Innate Immune System, and Oxidative Stress at the Maternal-Fetal Interface: An Overview

Moço¹,

Ramos²,

Silva³

et al. 2020

Translational Studies on Inflammation

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Despite the multifactorial etiology of prematurity, intra-amniotic infection is present in 25-40% of preterm pregnancies. Bacteria in amniotic cavity synthesize phospholipases associated with the production of prostaglandins that leads to rupture of fetal membranes and uterine contractions. Bacterial pathogen-associated molecular patterns (PAMPs) activate pattern recognition receptors (PRRs) such as Toll-like (TLRs) and NOD-like receptors (NLRs), triggering pathways that culminate in the production of cytokines that further increase prostaglandin release. Importantly, endogenous molecules called damage-associated molecular patterns (DAMPs) released under stressful conditions can also activate PRRs. Risk factors for both preterm labor (PTL) and preterm premature rupture of membranes (PPROM), including infection-induced inflammation, may cause an increase of ROS release and depletion of antioxidant defenses. In spite of the similarity between the pathophysiology of PTL and PPROM, there are significant differences regarding molecular mediators, degree of tissue damage, and oxidative stress present in these two conditions. PPROM seems to be a consequence of notable tissue damage resulting from chronic oxidative stress, while PTL is associated with minimal tissue degradation resulting from acute exposure and greater antioxidant status. A better understanding of prematurity pathophysiology and the differences between PTL and PPROM can benefit therapeutic approaches to prevent these important inflammatory syndromes.

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“…The placenta and decidua are the places where maternal and fetal tissues constitute a physical and immunologic barrier against invading infectious [29]. When microbes attack the maternal-fetal interface, the immune system induces inflammation, disrupting the immune balance between immune tolerance and immune response, endangering pregnancy [30].…”

Section: Discussionmentioning

confidence: 99%

Increased Toll-Like Receptor-Myeloid Differentiation Factor 88 Expression at the Maternal-Fetal Interface Is Associated with Spontaneous Abortion

Zhou²,

Jiang³

et al. 2017

Gynecol Obstet Invest

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Aims: Toll-like receptors (TLRs) form a group of pattern recognition receptors that play a major role in maintaining innate host immunity. Myeloid differentiation factor 88 (MyD88) is an adaptor molecule that is essential for signaling via the TLR family. To analyze the mechanism of the imbalance in the innate immune system mediated by TLRs-MyD88 in spontaneous abortion, we detected the expression of TLR-2, TLR-4, TLR-7, and MyD88 in placentae and deciduas. Methods: The expression of TLR-2, TLR-4, TLR-7, and MyD88 in the placentae and deciduas of abortion-prone mice (n = 10) and normal pregnant mice (n = 10) were analyzed by immunochemistry, western blot, and real-time polymerase chain reaction. Results: There were higher protein expression levels of TLR-2, TLR-4, TLR-7, and MyD88 in the placentae and deciduas in the abortion-prone group than in the normal pregnant group. However, TLR-2, TLR-4, and TLR-7 showed lower gene expression, while MyD88 manifested higher gene expression in placentae and deciduas of abortion-prone mice matings. Conclusions: TLR-2, TLR-4, TLR-7, and MyD88 were expressed in the placenta and decidua of both the abortion-prone pregnant and normal pregnant mice. The overexpression of TLRs may excessively activate the innate immune system mediated by MyD88, which is considered to be related to the pathogenesis of spontaneous abortion.

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NOD1 and NOD2 control the invasiveness of trophoblast cells via the MAPK/p38 signaling pathway in human first-trimester pregnancy

Cited by 31 publications

References 39 publications

Innate Immune System at the Maternal–Fetal Interface: Mechanisms of Disease and Targets of Therapy in Pregnancy Syndromes

Innate Immune System at the Maternal–Fetal Interface: Mechanisms of Disease and Targets of Therapy in Pregnancy Syndromes

Spontaneous Prematurity, Innate Immune System, and Oxidative Stress at the Maternal-Fetal Interface: An Overview

Increased Toll-Like Receptor-Myeloid Differentiation Factor 88 Expression at the Maternal-Fetal Interface Is Associated with Spontaneous Abortion

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