Cytokine secretion by human fetal membranes, decidua and placenta at term

Denison, Fiona C.; Kelly, Rodney W.; Calder, Andrew A.; Riley, Simon C.

doi:10.1093/humrep/13.12.3560

Cited by 131 publications

(82 citation statements)

References 36 publications

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“…During labour there is increased expression of proinflammatory mediators. These include pro-inflammatory cytokines, such as IL1b, IL6 and IL8 in the cervix, myometrium, foetal membranes and placenta (Denison et al 1998, Young et al 2002, Osman et al 2003; prostaglandins PGE 2 and PGF 2a in the foetal membranes and myometrium (Olson 2003); and matrix metalloproteinase 9 (MMP9) in the placenta and foetal membranes (Xu et al 2002). Regulation of these mediators facilitates tissue remodelling of the cervix, myometrial contractions and rupture of membranes, leading to successful delivery at term.…”

Section: Introductionmentioning

confidence: 99%

KLF5 regulates infection- and inflammation-induced pro-labour mediators in human myometrium

Lappas¹

2015

Reproduction

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The transcription factor Kruppel-like factor 5 (KLF5) has been shown to associate with nuclear factor kappa B (NFkB) to regulate genes involved in inflammation. However, there are no studies on the expression and regulation of KLF5 in the processes of human labour and delivery. Thus, the aims of this study were to determine the effect of i) human labour on KLF5 expression in both foetal membranes and myometrium; ii) the pro-inflammatory cytokine interleukin 1 beta (IL1b), bacterial product flagellin and the viral dsRNA analogue poly(I:C) on KLF5 expression and iii) KLF5 knockdown by siRNA in human myometrial primary cells on pro-inflammatory and pro-labour mediators. In foetal membranes, there was no effect of term or preterm labour on KLF5 expression. In myometrium, the term labour was associated with an increase in nuclear KLF5 protein expression. Moreover, KLF5 expression was also increased in myometrial cells treated with IL1b, flagellin or poly(IC), likely factors contributing to preterm birth. KLF5 silencing in myometrial cells significantly decreased IL1b-induced cytokine expression (IL6 and IL8 mRNA expression and release), COX2 mRNA expression, and subsequent release of prostaglandins PGE 2 and PGF 2a . KLF5 silencing also significantly reduced flagellin-and poly(I:C)-induced IL6 and IL8 mRNA expression. Lastly, IL1b-, flagellin-and poly(I:C)-stimulated NFkB transcriptional activity was significantly suppressed in KLF5-knockout myometrial cells. In conclusion, this study describes novel data in which KLF5 is increased in labouring myometrium, and KLF5 silencing decreased inflammation-and infection-induced pro-labour mediators.

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Section: Introductionmentioning

confidence: 99%

KLF5 regulates infection- and inflammation-induced pro-labour mediators in human myometrium

Lappas¹

2015

Reproduction

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“…Because RANTES is produced in human placental tissues (Denison et al, 1998) and can induce the migration of leukocytes and other cell types (Youngs et al, 1997), we speculated that this chemokine is a candidate for a DPPIV substrate that can affect trophoblastic migration. To substantiate this possibility, we initially examined the expression of RANTES receptors on trophoblasts.…”

Section: Introductionmentioning

confidence: 99%

“…Several chemokines, including CCR1 ligands, have been demonstrated in human placental tissue (Denison et al, 1998;Drake et al, 2001;Red-Horse et al, 2001). They are considered to be involved in either recruiting specific leukocyte populations to the feto-maternal interface or modulating trophoblastic function (Ishii et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Trophoblasts acquire a chemokine receptor, CCR1, as they differentiate towards invasive phenotype

et al. 2003

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At the human feto-maternal interface, trophoblasts differentiate towards extravillous trophoblasts (EVTs) and form the cell column. EVTs acquire invasive activity in the distal part of the cell column and begin to migrate into the maternal tissue. We previously reported that dipeptidyl peptidase IV(DPPIV) is expressed on EVTs in the proximal part of cell column and is involved in the inhibition of their migration. Because DPPIV has been shown to degrade several chemokines, we examined possible roles of chemokines in EVT migration.Immunohistochemistry demonstrated that C-C chemokine receptor 1 (CCR1) was hardly detected on cytotrophoblasts and syncytiotrophoblast but was expressed on EVTs in the cell column. In vitro, CCR1 protein was also present on the surface of EVTs that grew out from chorionic villous explants cultured under 20% O2. Chemokines that can bind to CCR1 (CCR1 ligands), such as regulated on activation, normal T cell expressed and secreted (RANTES) and macrophage inflammatory protein-1α (MIP-1α), were confirmed in the decidual tissues by RT-PCR and immunohistochemistry. These CCR1 ligands promoted the migration of the EVTs that were isolated from the explant cultures in vitro. These results indicate that CCR1 is expressed on trophoblasts as they differentiate to EVTs and that CCR1 ligands produced from the decidual tissue induce EVT migration.By contrast, CCR1 was scarcely expressed on EVTs that grew out from villous explants cultured in 1% O2, indicating that a relatively high oxygenic environment is needed to induce CCR1 expression. Moreover, CCR1 expression on the isolated EVTs was significantly reduced in the presence of decidua-conditioned medium. Such regulation of CCR1 by surrounding oxygenic and decidual environments supports a close correlation between EVT invasion and their expression of CCR1.This study demonstrates that trophoblasts acquire CCR1 as they differentiate to an invasive phenotype at the villus-anchoring sites and indicates a novel role for the chemokine-CCR1 system in the initial step of trophoblastic invasion towards the maternal tissue.

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“…Of particular interest is the chorionic membrane; it is the largest area of contact with the maternal tissues and it is the first tissue colonized by microbial pathogens during an ascending intrauterine infection. In vitro, human choriodecidua produces a 10-fold higher level of the proinflammatory cytokines TNF-␣ and MCP-1 than human amnion (7,8).…”

mentioning

confidence: 96%

The PDE4 Inhibitor Rolipram Prevents NF-κB Binding Activity and Proinflammatory Cytokine Release in Human Chorionic Cells

Hervé

Schmitz

Évain-Brion

et al. 2008

The Journal of Immunology

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Spontaneous preterm delivery is linked to intrauterine inflammation. Fetal membranes are involved in the inflammatory process as an important source of mediators, and the chorion leave produces high levels of the proinflammatory cytokine TNF-α when stimulated by LPS. The transcription factor NF-κB is the main regulator of this inflammatory process and controls the production of cytokines by the chorion leave. Phosphodiesterase 4 inhibitors are recognized for their anti-inflammatory and myorelaxant effects. The purpose of this study was to investigate whether PDE4 inhibition affects the LPS signaling in human cultured chorionic cells. We showed that these cells express TLR4, the main LPS receptor, and exhibit a predominant PDE4 activity. Upon LPS challenge, PDE4 activity increases concomitantly to the induction of the specific isoform PDE4B2 and chorionic cells secrete TNF-α. LPS induces the nuclear translocation of the NF-κB p65 subunit and the activation of three different NF-κB complexes in chorionic cells. The presence of the PDE4 inhibitor rolipram reduces the TNF-α production and the activation of the three NF-κB complexes. These data indicate that the PDE4 family interacts with the LPS signaling pathway during the inflammatory response of chorionic cells. PDE4 selective inhibitors may thus represent a new therapeutic approach in the management of inflammation-induced preterm delivery.

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Cytokine secretion by human fetal membranes, decidua and placenta at term

Cited by 131 publications

References 36 publications

KLF5 regulates infection- and inflammation-induced pro-labour mediators in human myometrium

KLF5 regulates infection- and inflammation-induced pro-labour mediators in human myometrium

Trophoblasts acquire a chemokine receptor, CCR1, as they differentiate towards invasive phenotype

The PDE4 Inhibitor Rolipram Prevents NF-κB Binding Activity and Proinflammatory Cytokine Release in Human Chorionic Cells

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