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Review: Impact of mediators present in amniotic fluid on preterm labour.

Abstract Preterm birth continues to be one of the most important issues in current obstetric medicine, being the single largest cause of perinatal morbidity and mortality. The signals that initiate preterm and term labour remain a mystery. Intrauterine inflammation with the secretion of cytokines is one of the accepted explanations for the mechanism of initiation of preterm labour. This review discusses the current understanding of the molecular mechanisms for the initiation of preterm labour, focusing chiefly on the role of intra-amniotic fluid mediators, whether endogenous or infection-induced, in the regulation of inflammatory response pathways associated with spontaneous preterm labour. Prostaglandins (PGs) are considered to be one of the key mediators of preterm labour, with the concentration of biologically active PGs in the amniotic fluid, particularly PGE(2) and PGF(2?), being significantly higher in women with preterm labour. Cytokines, such as interleukins and tumour necrosis factor alpha, additionally play a dominant role in preterm labour, particularly in association with infection. Elevated amniotic fluid concentrations of extracellular matrix mediators, including metalloproteases, are also implicated in the process of foetal membrane rupture in preterm labour. Allelic variations in the main amniotic fluid mediators may be the key to understanding the disparity in the rates of preterm birth between different ethnic populations. We also discuss the role of other potential mediators such as cell-adhesion molecules, nitric oxide and novel biomarkers found in the amniotic fluid.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title in vivo (athens, greece)
Publication Year Start
%A Vrachnis, Nikolaos; Karavolos, Stamatios; Iliodromiti, Zoe; Sifakis, Stavros; Siristatidis, Charalambos; Mastorakos, George; Creatsas, George
%T Review: Impact of mediators present in amniotic fluid on preterm labour.
%J In vivo (Athens, Greece), vol. 26, no. 5, pp. 799-812
%D 09/2012
%V 26
%N 5
%M eng
%B Preterm birth continues to be one of the most important issues in current obstetric medicine, being the single largest cause of perinatal morbidity and mortality. The signals that initiate preterm and term labour remain a mystery. Intrauterine inflammation with the secretion of cytokines is one of the accepted explanations for the mechanism of initiation of preterm labour. This review discusses the current understanding of the molecular mechanisms for the initiation of preterm labour, focusing chiefly on the role of intra-amniotic fluid mediators, whether endogenous or infection-induced, in the regulation of inflammatory response pathways associated with spontaneous preterm labour. Prostaglandins (PGs) are considered to be one of the key mediators of preterm labour, with the concentration of biologically active PGs in the amniotic fluid, particularly PGE(2) and PGF(2?), being significantly higher in women with preterm labour. Cytokines, such as interleukins and tumour necrosis factor alpha, additionally play a dominant role in preterm labour, particularly in association with infection. Elevated amniotic fluid concentrations of extracellular matrix mediators, including metalloproteases, are also implicated in the process of foetal membrane rupture in preterm labour. Allelic variations in the main amniotic fluid mediators may be the key to understanding the disparity in the rates of preterm birth between different ethnic populations. We also discuss the role of other potential mediators such as cell-adhesion molecules, nitric oxide and novel biomarkers found in the amniotic fluid.
%K Amniotic Fluid, Animals, Cell Adhesion Molecules, Extracellular Matrix Proteins, Female, Humans, Inflammation Mediators, Labor, Obstetric, Pregnancy, Premature Birth
%P 799
%L 812
%W PHY
%G AUTHOR
%R 2012.......26..799V

@Article{Vrachnis2012,
author="Vrachnis, Nikolaos
and Karavolos, Stamatios
and Iliodromiti, Zoe
and Sifakis, Stavros
and Siristatidis, Charalambos
and Mastorakos, George
and Creatsas, George",
title="Review: Impact of mediators present in amniotic fluid on preterm labour.",
journal="In vivo (Athens, Greece)",
year="2012",
month="Sep/Oct",
volume="26",
number="5",
pages="799--812",
keywords="Amniotic Fluid",
keywords="Animals",
keywords="Cell Adhesion Molecules",
keywords="Extracellular Matrix Proteins",
keywords="Female",
keywords="Humans",
keywords="Inflammation Mediators",
keywords="Labor, Obstetric",
keywords="Pregnancy",
keywords="Premature Birth",
abstract="Preterm birth continues to be one of the most important issues in current obstetric medicine, being the single largest cause of perinatal morbidity and mortality. The signals that initiate preterm and term labour remain a mystery. Intrauterine inflammation with the secretion of cytokines is one of the accepted explanations for the mechanism of initiation of preterm labour. This review discusses the current understanding of the molecular mechanisms for the initiation of preterm labour, focusing chiefly on the role of intra-amniotic fluid mediators, whether endogenous or infection-induced, in the regulation of inflammatory response pathways associated with spontaneous preterm labour. Prostaglandins (PGs) are considered to be one of the key mediators of preterm labour, with the concentration of biologically active PGs in the amniotic fluid, particularly PGE(2) and PGF(2$\alpha$), being significantly higher in women with preterm labour. Cytokines, such as interleukins and tumour necrosis factor alpha, additionally play a dominant role in preterm labour, particularly in association with infection. Elevated amniotic fluid concentrations of extracellular matrix mediators, including metalloproteases, are also implicated in the process of foetal membrane rupture in preterm labour. Allelic variations in the main amniotic fluid mediators may be the key to understanding the disparity in the rates of preterm birth between different ethnic populations. We also discuss the role of other potential mediators such as cell-adhesion molecules, nitric oxide and novel biomarkers found in the amniotic fluid.",
issn="1791-7549",
url="http://www.ncbi.nlm.nih.gov/pubmed/22949593",
language="eng"
}

%0 Journal Article
%T Review: Impact of mediators present in amniotic fluid on preterm labour.
%A Vrachnis, Nikolaos
%A Karavolos, Stamatios
%A Iliodromiti, Zoe
%A Sifakis, Stavros
%A Siristatidis, Charalambos
%A Mastorakos, George
%A Creatsas, George
%J In vivo (Athens, Greece)
%D 2012
%8 Sep/Oct
%V 26
%N 5
%@ 1791-7549
%G eng
%F Vrachnis2012
%X Preterm birth continues to be one of the most important issues in current obstetric medicine, being the single largest cause of perinatal morbidity and mortality. The signals that initiate preterm and term labour remain a mystery. Intrauterine inflammation with the secretion of cytokines is one of the accepted explanations for the mechanism of initiation of preterm labour. This review discusses the current understanding of the molecular mechanisms for the initiation of preterm labour, focusing chiefly on the role of intra-amniotic fluid mediators, whether endogenous or infection-induced, in the regulation of inflammatory response pathways associated with spontaneous preterm labour. Prostaglandins (PGs) are considered to be one of the key mediators of preterm labour, with the concentration of biologically active PGs in the amniotic fluid, particularly PGE(2) and PGF(2?), being significantly higher in women with preterm labour. Cytokines, such as interleukins and tumour necrosis factor alpha, additionally play a dominant role in preterm labour, particularly in association with infection. Elevated amniotic fluid concentrations of extracellular matrix mediators, including metalloproteases, are also implicated in the process of foetal membrane rupture in preterm labour. Allelic variations in the main amniotic fluid mediators may be the key to understanding the disparity in the rates of preterm birth between different ethnic populations. We also discuss the role of other potential mediators such as cell-adhesion molecules, nitric oxide and novel biomarkers found in the amniotic fluid.
%K Amniotic Fluid
%K Animals
%K Cell Adhesion Molecules
%K Extracellular Matrix Proteins
%K Female
%K Humans
%K Inflammation Mediators
%K Labor, Obstetric
%K Pregnancy
%K Premature Birth
%U http://www.ncbi.nlm.nih.gov/pubmed/22949593
%P 799-812

PT Journal
AU Vrachnis, N
   Karavolos, S
   Iliodromiti, Z
   Sifakis, S
   Siristatidis, C
   Mastorakos, G
   Creatsas, G
TI Review: Impact of mediators present in amniotic fluid on preterm labour.
SO In vivo (Athens, Greece)
JI In Vivo
PD Sep/Oct
PY 2012
BP 799
EP 812
VL 26
IS 5
LA eng
DE Amniotic Fluid; Animals; Cell Adhesion Molecules; Extracellular Matrix Proteins; Female; Humans; Inflammation Mediators; Labor, Obstetric; Pregnancy; Premature Birth
AB Preterm birth continues to be one of the most important issues in current obstetric medicine, being the single largest cause of perinatal morbidity and mortality. The signals that initiate preterm and term labour remain a mystery. Intrauterine inflammation with the secretion of cytokines is one of the accepted explanations for the mechanism of initiation of preterm labour. This review discusses the current understanding of the molecular mechanisms for the initiation of preterm labour, focusing chiefly on the role of intra-amniotic fluid mediators, whether endogenous or infection-induced, in the regulation of inflammatory response pathways associated with spontaneous preterm labour. Prostaglandins (PGs) are considered to be one of the key mediators of preterm labour, with the concentration of biologically active PGs in the amniotic fluid, particularly PGE(2) and PGF(2?), being significantly higher in women with preterm labour. Cytokines, such as interleukins and tumour necrosis factor alpha, additionally play a dominant role in preterm labour, particularly in association with infection. Elevated amniotic fluid concentrations of extracellular matrix mediators, including metalloproteases, are also implicated in the process of foetal membrane rupture in preterm labour. Allelic variations in the main amniotic fluid mediators may be the key to understanding the disparity in the rates of preterm birth between different ethnic populations. We also discuss the role of other potential mediators such as cell-adhesion molecules, nitric oxide and novel biomarkers found in the amniotic fluid.
ER


TY  - JOUR
AU  - Vrachnis, Nikolaos
AU  - Karavolos, Stamatios
AU  - Iliodromiti, Zoe
AU  - Sifakis, Stavros
AU  - Siristatidis, Charalambos
AU  - Mastorakos, George
AU  - Creatsas, George
PY  - 2012/Sep/Oct/
TI  - Review: Impact of mediators present in amniotic fluid on preterm labour.
T2  - In Vivo
JO  - In vivo (Athens, Greece)
SP  - 799
EP  - 812
VL  - 26
IS  - 5
KW  - Amniotic Fluid
KW  - Animals
KW  - Cell Adhesion Molecules
KW  - Extracellular Matrix Proteins
KW  - Female
KW  - Humans
KW  - Inflammation Mediators
KW  - Labor, Obstetric
KW  - Pregnancy
KW  - Premature Birth
N2  - Preterm birth continues to be one of the most important issues in current obstetric medicine, being the single largest cause of perinatal morbidity and mortality. The signals that initiate preterm and term labour remain a mystery. Intrauterine inflammation with the secretion of cytokines is one of the accepted explanations for the mechanism of initiation of preterm labour. This review discusses the current understanding of the molecular mechanisms for the initiation of preterm labour, focusing chiefly on the role of intra-amniotic fluid mediators, whether endogenous or infection-induced, in the regulation of inflammatory response pathways associated with spontaneous preterm labour. Prostaglandins (PGs) are considered to be one of the key mediators of preterm labour, with the concentration of biologically active PGs in the amniotic fluid, particularly PGE(2) and PGF(2?), being significantly higher in women with preterm labour. Cytokines, such as interleukins and tumour necrosis factor alpha, additionally play a dominant role in preterm labour, particularly in association with infection. Elevated amniotic fluid concentrations of extracellular matrix mediators, including metalloproteases, are also implicated in the process of foetal membrane rupture in preterm labour. Allelic variations in the main amniotic fluid mediators may be the key to understanding the disparity in the rates of preterm birth between different ethnic populations. We also discuss the role of other potential mediators such as cell-adhesion molecules, nitric oxide and novel biomarkers found in the amniotic fluid.
SN  - 1791-7549
UR  - http://www.ncbi.nlm.nih.gov/pubmed/22949593
ID  - Vrachnis2012
ER  -