Increased matrix metalloproteinase activity and reduced tissue inhibitor of metalloproteinases-1 levels in amniotic fluids from pregnancies complicated by premature rupture of membranes

Vadillo-Ortega, Felipe; Hernández, Antonia; González-Ávila, Georgina; Bermejo, Luisa; Iwata, Kazushi; Strauss, Jerome F.

doi:10.1016/s0002-9378(96)70687-7

Cited by 161 publications

(76 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…As the amniochorionic membranes are connective tissue structures, many studies have focused on the expression of matrix-degrading enzymes in the amniochorionic membranes. In support of this, increases in amniotic fluid matrix metalloproteases (MMPs) (19 -21) as well as decreases in tissue inhibitors of MMPs have been reported for women with PPROM (22). Nevertheless, similar findings are observed for normal spontaneous term delivery and infection-induced PL and PPROM.…”

Section: Discussionmentioning

confidence: 66%

Prolonged Preterm Rupture of Fetal Membranes, a Consequence of an Increased Maternal Anti-fetal T Cell Responsiveness

et al. 2005

View full text Add to dashboard Cite

A fetus, although semi-allogeneic, is usually accepted by the maternal immune system. However, complications, including alloresponsive mechanisms, are thought to be potentially detrimental for a successful pregnancy. Therefore, we compared allogeneic T cell responses of nonpregnant women with the response of healthy pregnant women and pregnant women who have various gestation-associated diseases. Peripheral blood mononuclear cells (PBMCs) of all three groups were stimulated with PBMCs from unrelated volunteers. Pregnant women had significantly reduced stimulation indices (SIs) compared with nonpregnant women. Exposing PBMCs from pregnant women to PBMCs of their own fetus led to a further significant decrease of SIs. Among the two groups of pregnant individuals, SIs of women with prolonged preterm rupture of fetal membranes (PPROM) were significantly higher when the maternal PBMCs were stimulated with PBMCs of their own fetus. This phenomenon could not be observed after stimulation with PBMCs from unrelated volunteers. In addition, an increased humoral immune response was assessed for women with PPROM in comparison with women with uncontrollable preterm labor. Our results revealed a strongly reduced allogeneic T cell response of PBMCs from pregnant women that was further down-regulated when PBMCs from their own fetus were used as stimulators. By contrast, data from women with PPROM suggest an increased maternal T cell response specifically toward the fetal HLA antigens. During pregnancy the maternal immune system is confronted with paternal allo-antigens expressed by the fetal tissues. Therefore, maternal immune rejection processes toward fetal HLA antigens may represent a major cause of complications, such as uncontrollable preterm labor (PL), prolonged preterm rupture of fetal membranes (PPROM), pregnancyinduced hypertensive diseases [preeclampsia; hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome] or intrauterine growth restriction (IUGR). Several local mechanisms that act at the maternal-fetal interface to protect the fetus from maternal immune attack are known (1). In addition, mechanisms that induce peripheral immune tolerance to the fetus seem to be of equal if not of greater importance for successful course of pregnancy.One such mechanism is most possibly the induction of CD25ϩCD4ϩ T regulatory cells, a specialized T cell population that was shown not only to suppress autoaggressive immune responses (2) but also to prevent graft rejection as a result of induction of transplantation tolerance (3). Pregnancyinduced expansion of these regulatory T cells occurs in both mice (4) and humans (5). These cells were able to suppress the allogeneic T cell response directed against the fetus (4). Recently, it was reported that normal human pregnancy also is Received November 17, 2004; accepted February 11, 2005

show abstract

Section: Discussionmentioning

confidence: 66%

Prolonged Preterm Rupture of Fetal Membranes, a Consequence of an Increased Maternal Anti-fetal T Cell Responsiveness

et al. 2005

View full text Add to dashboard Cite

show abstract

“…A similar situation was observed for PGE 2 , where plasma conditioned with live U. urea- The amniochorion secretes MMP-9 in response to the addition of plasma conditioned with GBS. Elevation of MMP-9 in amniotic fluid and the amniochorion has been implicated in both physiologic and pathological rupture of the fetal membranes (22,47,48). We evaluated if plasma samples derived from the initial interaction between bacteria and placental blood stimulated the secretion of MMP-9 by the amniochorion.…”

Section: Resultsmentioning

confidence: 99%

Interaction between Pathogenic Bacteria and Intrauterine Leukocytes Triggers Alternative Molecular Signaling Cascades Leading to Labor in Women

et al. 2010

Self Cite

View full text Add to dashboard Cite

Increased risk of preterm labor has been linked to cervicovaginal infection with Ureaplasma urealyticum and group B streptococci. Although various experimental models have been developed to study the role of amniochorion infection in preterm labor, they typically exclude the initial interaction between intrauterine leukocytes (recruited from decidual vessels into the avascular fetal membranes) and infecting bacteria. In this work, we ascertained whether inflammatory molecules secreted by bacterium-activated intrauterine leukocytes stimulate the amniochorion production of mediators involved in human labor. Using a two-step process beginning with placental circulating leukocytes as a proxy for intrauterine leukocytes, we found that coincubation of amniochorion explants with plasma from placental whole blood preincubated with group B streptococci resulted in a significant increase in tumor necrosis factor alpha (TNF-␣) and matrix metalloproteinase 9 (MMP-9) levels in tissue. Extensive changes in the connective tissue arrangement and a decrease in collagen content demonstrated the degradation of the extracellular matrix following this treatment. In contrast, plasma from blood preconditioned with U. urealyticum induced a highly significant secretion of interleukin-1␤ (IL-1␤) and prostaglandin E 2 (PGE 2 ) by the amniochorion without changes in the extracellular matrix organization or content. These data demonstrate that group B streptococci induce degradation of the amniochorion as a result of MMP-9 production, probably via TNF-␣, whereas U. urealyticum stimulates the secretion of PGE 2 , probably via IL-1␤, potentially stimulating myometrial contraction. Our study provides novel evidence that the immunological cells circulating within the uterine microenvironment respond differentially to an infectious agent, triggering alternative molecular signaling pathways leading to human labor.

show abstract

“…At the same time the level of TIMP-1 was reduced in the cervical area of PROM as well as pre-term derived membranes, in comparison to the placental area. It was also lower than in corresponding area of membranes [20,21]. Another group reported elevated TIMP-1 levels in amniotic fluid samples derived from deliveries complicated with PROM, nevertheless this study did not include MMP-9 assessment or MMP-9/TIMP-1 ratio [22].…”

Section: Discussionmentioning

confidence: 71%

The MMP-9/TIMP-1 imbalance and the reduced level of TGF-β in the cervical area of amniotic membrane is a possible risk factor of PROM and premature labor — proof-of-concept study

et al. 2017

View full text Add to dashboard Cite

Objectives:To assess the level MMP-9, TIMP-1 and TGF-β in placental and cervical region of amniotic membranes derived from at-term, pre-term and PROM deliveries.Material and methods: 14 amniotic membranes have been assessed; the quantitative analysis of MMP-9, TGF-β and TIMP-1 was assayed using respective Quantikine Immunoassay Kit. Results:The MMP-9 level in PROM samples was similar to the level of MMP-9 in at-term membranes and comparable between the cervical and placental region of these membranes. The concentration of TGF-β and TIMP-1 was decreased in the cervical area of AM derived from deliveries complicated with PROM. Conclusion:The MMP9/TIMP-1 imbalance, as well as the reduced level of TGF-β may be possible risk factors of pre-term labor and PROM.

show abstract

Increased matrix metalloproteinase activity and reduced tissue inhibitor of metalloproteinases-1 levels in amniotic fluids from pregnancies complicated by premature rupture of membranes

Cited by 161 publications

References 17 publications

Prolonged Preterm Rupture of Fetal Membranes, a Consequence of an Increased Maternal Anti-fetal T Cell Responsiveness

Prolonged Preterm Rupture of Fetal Membranes, a Consequence of an Increased Maternal Anti-fetal T Cell Responsiveness

Interaction between Pathogenic Bacteria and Intrauterine Leukocytes Triggers Alternative Molecular Signaling Cascades Leading to Labor in Women

The MMP-9/TIMP-1 imbalance and the reduced level of TGF-β in the cervical area of amniotic membrane is a possible risk factor of PROM and premature labor — proof-of-concept study

Contact Info

Product

Resources

About