Interleukin-1β and bacterial endotoxin change the metabolism of prostaglandins E2 and F2α in intact term fetal membranes

Brown, Naoko; Alvi, Sabah; Elder, M. G.; Bennett, Phillip R.; Sullivan, Mark

doi:10.1016/s0143-4004(98)90024-8

Cited by 46 publications

(29 citation statements)

References 29 publications

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“…One of these is PTGS2, which was shown to be selectively induced by flagellin and MALP-2 in amniotic epithelial cells. These data expand previous reports indicating that bacterial products affect PG synthesis by fetal membranes (36)(37)(38)(39)(40). We then hypothesized that the PGs consequently produced have the ability to induce the production of MMP.…”

Section: Discussionsupporting

confidence: 88%

Functional Screening of TLRs in Human Amniotic Epithelial Cells

Gillaux

Méhats

Vaiman

et al. 2011

The Journal of Immunology

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Intrauterine infection is a major cause of spontaneous preterm birth. Amniotic epithelial cells represent the first line of defense against intra-amniotic bacteria. We hypothesize that this epithelial cell barrier is able to recognize and respond to pathogens through the function of TLRs, which are crucial regulators of the innate immune system. In this study, we describe the expression of transcripts for TLR1–TLR10 in human amniotic epithelial cells. We show that amniotic epithelial cells express functional TLR5, TLR6/2, and TLR4. Activation by TLR5 and TLR6/2 agonists produces IL-6 and IL-8, concomitantly with the activation of NF-κB signaling pathway, matrix metalloproteinase-9 induction, and PTGS2 expression. In contrast, TLR4 activation reduced amniotic epithelial cell viability and induced cell apoptosis evidenced by an elevated Bax/Bcl-2 ratio and cleavage of caspase-3. These data suggest specific TLR-mediated functions in human amniotic epithelial cells for initiating different immune responses, which ultimately may lead to preterm birth.

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Section: Discussionsupporting

confidence: 88%

Functional Screening of TLRs in Human Amniotic Epithelial Cells

Gillaux

Méhats

Vaiman

et al. 2011

The Journal of Immunology

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“…3), which reinforces the reduced enzyme activity that we have previously observed. In accordance with this, Brown et al (1998) were able to detect a significant decrease in the levels of PG metabolites following incubation with LPS in explants from human fetal membranes. Based on these results, we suggest that in our model, the mechanism by which LPS regulates the levels of PGE 2 is by increasing and decreasing PGE synthase activity and HPGD protein expression respectively.…”

Section: Discussionsupporting

confidence: 79%

“…Expression and activity of 15-PGDH have been demonstrated in reproductive tissues of different species (Casey et al 1980, Kankofer 1999, Gao et al 2007. LPS treatment decreases activity of 15-PGDH in mouse and human fetal membranes at term (Brown et al 1998, Wang & Hirsch 2003 and alters Hpgd mRNA and protein levels in mouse and rat lung during sepsis (Hahn et al 1998, Ivanov & Romanovsky 2004). …”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide-induced murine embryonic resorption involves nitric oxide-mediated inhibition of the NAD+-dependent 15-hydroxyprostaglandin dehydrogenase

Aisemberg¹,

Bariani²,

Vercelli³

et al. 2012

Reproduction

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The initial inactivation of prostaglandins (PGs) is mediated by 15-hydroxyprostaglandin dehydrogenase (15-PGDH). PGs are potent mediators of several biological processes, including inflammation and reproduction. In uterus, PGs play a key role in infectioninduced pregnancy loss, in which concentration of this mediator increased. This process is accompanied with the induction of nitric oxide synthase expression and a marked increase in uterine levels of nitric oxide. There is no information concerning nitric oxide contribution to potential changes in PG catabolism, but experimental evidence suggests that nitric oxide modulates PG pathways. The specific objectives of the study were to evaluate the protein expression of HPGD (15-PGDH) and to characterize the nitric oxide-dependent regulation of this enzyme in a model of lipopolysaccharide (LPS)-induced embryonic resorption. Results show that LPS decreased HPGD protein expression and augmented PGE synthase activity; therefore, PGE 2 levels increased in uterus in this inflammatory condition. Just as LPS, the treatment with a nitric oxide donor diminished HPGD protein expression in uterine tissue. In contrast, the inhibition of nitric oxide synthesis both in control and in LPS-treated mice increased 15-PGDH levels. Also, we have found that this enzyme and PGE 2 levels are not modulated by peroxynitrite, an oxidant agent derived from nitric oxide. This study suggests that LPS and nitric oxide promote a decrease in the ability of the uterus for PG catabolism during bacterially triggered pregnancy loss in mice.

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“…The IL-6 level has been proposed as a marker for the prediction of preterm delivery (24). TNF-␣, IL-1␤, and IL-6 can induce the production of both prostaglandins and metalloproteases leading to preterm delivery (19,20). Double knockouts for TNF-␣ and IL-1␤ receptors are refractory to bacterially induced preterm labor (22).…”

Section: Discussionmentioning

confidence: 99%

“…To assess that the onset of preterm labor in LPS-injected dams was concomitant to an intrauterine inflammation and that this phenomenon was prevented in the presence of rolipram, we measured the concentration of cytokines in amniotic fluids, namely TNF-␣, IL-1␤, IL-6, and IL-10, which have been reported to be involved in inflammation-induced preterm delivery (19,20). As depicted in Fig.…”

Section: Decrease Of Inflammation-induced Cytokines Level Rises In Ammentioning

confidence: 99%

PDE4 Inhibition Prevents Preterm Delivery Induced by an Intrauterine Inflammation

Schmitz

Souil

Hervé

et al. 2007

The Journal of Immunology

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The aim of this study was to explore the anti-inflammatory properties of phosphodiesterase-4 (PDE4) inhibitors in vivo and their potential ability to prevent inflammation-induced preterm delivery. Indeed, intrauterine inflammation is the major etiology of very preterm delivery, the leading cause of neonatal mortality and morbidity. Intrauterine injection of Escherichia coli LPS in 15-day-pregnant mice induced an increase of PDE4 activity and PDE4B expression at the maternofetal interface, a rise of amniotic fluid levels of TNF-α, IL-1β, IL-6, and IL-10 and provoked massive preterm delivery and fetal demise. Selective PDE4 inhibition by rolipram prevented the rise in the proinflammatory cytokines. Following the nuclear translocation of the transcription factor NFκB, as a marker of cellular activation after the inflammatory challenge, showed a time-dependent sequential activation of the gestational tissues, from the uterine mesometrial to the fetal compartment, particularly in the glycogen-trophoblastic cells of the placenta. This activation was disrupted by PDE4 inhibition, and inflammation-induced preterm delivery and fetal demise were prevented. PDE4 selective inhibitors may thus represent a novel effective treatment to delay inflammation-induced preterm delivery and to prevent adverse outcomes in infants.

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Interleukin-1β and bacterial endotoxin change the metabolism of prostaglandins E2 and F2α in intact term fetal membranes

Cited by 46 publications

References 29 publications

Functional Screening of TLRs in Human Amniotic Epithelial Cells

Functional Screening of TLRs in Human Amniotic Epithelial Cells

Lipopolysaccharide-induced murine embryonic resorption involves nitric oxide-mediated inhibition of the NAD+-dependent 15-hydroxyprostaglandin dehydrogenase

PDE4 Inhibition Prevents Preterm Delivery Induced by an Intrauterine Inflammation

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