Fetal sex and preterm birth
Abstract Rates of preterm birth vary between different populations and ethnic groups. Epidemiologic studies have suggested that the incidence of preterm birth is also higher in pregnancies carrying a male fetus; the male:female difference is greater in earlier preterm pregnancy. Placental or chorion...
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| Veröffentlicht in: | Placenta (Eastbourne) 2013-02, Vol.34 (2), p.95-99 |
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| creator | Challis, J Newnham, J Petraglia, F Yeganegi, M Bocking, A |
| description | Abstract Rates of preterm birth vary between different populations and ethnic groups. Epidemiologic studies have suggested that the incidence of preterm birth is also higher in pregnancies carrying a male fetus; the male:female difference is greater in earlier preterm pregnancy. Placental or chorion trophoblast cells from pregnancies with a male fetus produced more pro-inflammatory TNFα in response to LPS stimulation and less anti-inflammatory IL-10 and granulocyte colony stimulating factor (G-CSF) than cells from pregnancies with a female fetus, more prostaglandin synthase (PTGS-2) and less prostaglandin dehydrogenase (PGDH). These results suggest that in the presence of a male fetus the trophoblast has the potential to generate a more pro-inflammatory environment. Maturation of the fetal hypothalamic–pituitary–adrenal axis and expression of placental genes, particularly 11β hydroxysteroid dehydrogenase-2 are also expressed in a sex dependent manner, consistent with the sex-biasing influences on gene networks. Sex differences in these activities may affect clinical outcomes of pre- and post-dates pregnancies and fetal/newborn wellbeing. These factors need consideration in studies of placental function and in the development of personalized strategies for the diagnosis of preterm labor and postnatal health. |
| doi_str_mv | 10.1016/j.placenta.2012.11.007 |
| format | Article |
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Epidemiologic studies have suggested that the incidence of preterm birth is also higher in pregnancies carrying a male fetus; the male:female difference is greater in earlier preterm pregnancy. Placental or chorion trophoblast cells from pregnancies with a male fetus produced more pro-inflammatory TNFα in response to LPS stimulation and less anti-inflammatory IL-10 and granulocyte colony stimulating factor (G-CSF) than cells from pregnancies with a female fetus, more prostaglandin synthase (PTGS-2) and less prostaglandin dehydrogenase (PGDH). These results suggest that in the presence of a male fetus the trophoblast has the potential to generate a more pro-inflammatory environment. Maturation of the fetal hypothalamic–pituitary–adrenal axis and expression of placental genes, particularly 11β hydroxysteroid dehydrogenase-2 are also expressed in a sex dependent manner, consistent with the sex-biasing influences on gene networks. Sex differences in these activities may affect clinical outcomes of pre- and post-dates pregnancies and fetal/newborn wellbeing. These factors need consideration in studies of placental function and in the development of personalized strategies for the diagnosis of preterm labor and postnatal health.</description><identifier>ISSN: 0143-4004</identifier><identifier>EISSN: 1532-3102</identifier><identifier>DOI: 10.1016/j.placenta.2012.11.007</identifier><identifier>PMID: 23261268</identifier><identifier>CODEN: PLACDF</identifier><language>eng</language><publisher>Kidlington: Elsevier Ltd</publisher><subject>11-beta-Hydroxysteroid Dehydrogenase Type 2 - metabolism ; Biological and medical sciences ; Cytokines ; Embryology: invertebrates and vertebrates. Teratology ; Female ; Fetal sex ; Fetus - physiopathology ; Fundamental and applied biological sciences. Psychology ; HPA axis ; Humans ; Hypothalamo-Hypophyseal System - physiopathology ; Infant, Newborn ; Inflammation Mediators - physiology ; Internal Medicine ; Male ; Obstetric Labor, Premature - etiology ; Obstetric Labor, Premature - physiopathology ; Obstetrics and Gynecology ; Pituitary-Adrenal System - physiopathology ; Placenta ; Placenta - physiopathology ; Pregnancy ; Pregnancy Complications, Infectious - etiology ; Pregnancy Complications, Infectious - physiopathology ; Pregnancy. Parturition. Lactation ; Premature Birth - etiology ; Premature Birth - physiopathology ; Preterm birth ; Probiotics - therapeutic use ; Risk Factors ; Sex Characteristics ; Stress, Physiological ; Trophoblasts - physiology ; Vertebrates: reproduction</subject><ispartof>Placenta (Eastbourne), 2013-02, Vol.34 (2), p.95-99</ispartof><rights>Elsevier Ltd</rights><rights>2012 Elsevier Ltd</rights><rights>2014 INIST-CNRS</rights><rights>Copyright © 2012 Elsevier Ltd. 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Epidemiologic studies have suggested that the incidence of preterm birth is also higher in pregnancies carrying a male fetus; the male:female difference is greater in earlier preterm pregnancy. Placental or chorion trophoblast cells from pregnancies with a male fetus produced more pro-inflammatory TNFα in response to LPS stimulation and less anti-inflammatory IL-10 and granulocyte colony stimulating factor (G-CSF) than cells from pregnancies with a female fetus, more prostaglandin synthase (PTGS-2) and less prostaglandin dehydrogenase (PGDH). These results suggest that in the presence of a male fetus the trophoblast has the potential to generate a more pro-inflammatory environment. Maturation of the fetal hypothalamic–pituitary–adrenal axis and expression of placental genes, particularly 11β hydroxysteroid dehydrogenase-2 are also expressed in a sex dependent manner, consistent with the sex-biasing influences on gene networks. Sex differences in these activities may affect clinical outcomes of pre- and post-dates pregnancies and fetal/newborn wellbeing. These factors need consideration in studies of placental function and in the development of personalized strategies for the diagnosis of preterm labor and postnatal health.</description><subject>11-beta-Hydroxysteroid Dehydrogenase Type 2 - metabolism</subject><subject>Biological and medical sciences</subject><subject>Cytokines</subject><subject>Embryology: invertebrates and vertebrates. Teratology</subject><subject>Female</subject><subject>Fetal sex</subject><subject>Fetus - physiopathology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>HPA axis</subject><subject>Humans</subject><subject>Hypothalamo-Hypophyseal System - physiopathology</subject><subject>Infant, Newborn</subject><subject>Inflammation Mediators - physiology</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Obstetric Labor, Premature - etiology</subject><subject>Obstetric Labor, Premature - physiopathology</subject><subject>Obstetrics and Gynecology</subject><subject>Pituitary-Adrenal System - physiopathology</subject><subject>Placenta</subject><subject>Placenta - physiopathology</subject><subject>Pregnancy</subject><subject>Pregnancy Complications, Infectious - etiology</subject><subject>Pregnancy Complications, Infectious - physiopathology</subject><subject>Pregnancy. Parturition. Lactation</subject><subject>Premature Birth - etiology</subject><subject>Premature Birth - physiopathology</subject><subject>Preterm birth</subject><subject>Probiotics - therapeutic use</subject><subject>Risk Factors</subject><subject>Sex Characteristics</subject><subject>Stress, Physiological</subject><subject>Trophoblasts - physiology</subject><subject>Vertebrates: reproduction</subject><issn>0143-4004</issn><issn>1532-3102</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcFq20AQhpfS0DhunyBgfCnkImVmdiWtLqUlxEnAkEOS87Jejci6suTuyqF--0jYaaCXXGYu3z8zfCPEDCFFwPxynW4b67jtbUqAlCKmAMUnMcFMUiIR6LOYACqZKAB1Ks5iXANAqZC-iFOSlCPleiLOF9zbZh7579y21XwbuOewma986J-_ipPaNpG_HftUPC2uH69uk-X9zd3Vr2XiVCb7ZFUqLiot67zQqBHqTK5I6pxcSap0LpNFJlUtZV5l5CrpNLiBL6GgElCCnIqLw9xt6P7sOPZm46PjprEtd7tokLQirbNyRPMD6kIXY-DabIPf2LA3CGYUY9bmTYwZxRhEM4gZgrPjjt1qw9W_2JuJAfh-BGx0tqmDbZ2P71yuMxzPnYqfB44HIy-eg4nOc-u48oFdb6rOf3zLj_9GuMa3ftj6m_cc190utINvgyaSAfMwvnH8ItJQFIF8BUmrlRA</recordid><startdate>20130201</startdate><enddate>20130201</enddate><creator>Challis, J</creator><creator>Newnham, J</creator><creator>Petraglia, F</creator><creator>Yeganegi, M</creator><creator>Bocking, A</creator><general>Elsevier Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20130201</creationdate><title>Fetal sex and preterm birth</title><author>Challis, J ; Newnham, J ; Petraglia, F ; Yeganegi, M ; Bocking, A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c453t-b94e7d83f6781810f53b23862c9249cc537534f336d52cd3c80c7d89072901303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>11-beta-Hydroxysteroid Dehydrogenase Type 2 - metabolism</topic><topic>Biological and medical sciences</topic><topic>Cytokines</topic><topic>Embryology: invertebrates and vertebrates. Teratology</topic><topic>Female</topic><topic>Fetal sex</topic><topic>Fetus - physiopathology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>HPA axis</topic><topic>Humans</topic><topic>Hypothalamo-Hypophyseal System - physiopathology</topic><topic>Infant, Newborn</topic><topic>Inflammation Mediators - physiology</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Obstetric Labor, Premature - etiology</topic><topic>Obstetric Labor, Premature - physiopathology</topic><topic>Obstetrics and Gynecology</topic><topic>Pituitary-Adrenal System - physiopathology</topic><topic>Placenta</topic><topic>Placenta - physiopathology</topic><topic>Pregnancy</topic><topic>Pregnancy Complications, Infectious - etiology</topic><topic>Pregnancy Complications, Infectious - physiopathology</topic><topic>Pregnancy. Parturition. Lactation</topic><topic>Premature Birth - etiology</topic><topic>Premature Birth - physiopathology</topic><topic>Preterm birth</topic><topic>Probiotics - therapeutic use</topic><topic>Risk Factors</topic><topic>Sex Characteristics</topic><topic>Stress, Physiological</topic><topic>Trophoblasts - physiology</topic><topic>Vertebrates: reproduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Challis, J</creatorcontrib><creatorcontrib>Newnham, J</creatorcontrib><creatorcontrib>Petraglia, F</creatorcontrib><creatorcontrib>Yeganegi, M</creatorcontrib><creatorcontrib>Bocking, A</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Placenta (Eastbourne)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Challis, J</au><au>Newnham, J</au><au>Petraglia, F</au><au>Yeganegi, M</au><au>Bocking, A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fetal sex and preterm birth</atitle><jtitle>Placenta (Eastbourne)</jtitle><addtitle>Placenta</addtitle><date>2013-02-01</date><risdate>2013</risdate><volume>34</volume><issue>2</issue><spage>95</spage><epage>99</epage><pages>95-99</pages><issn>0143-4004</issn><eissn>1532-3102</eissn><coden>PLACDF</coden><abstract>Abstract Rates of preterm birth vary between different populations and ethnic groups. Epidemiologic studies have suggested that the incidence of preterm birth is also higher in pregnancies carrying a male fetus; the male:female difference is greater in earlier preterm pregnancy. Placental or chorion trophoblast cells from pregnancies with a male fetus produced more pro-inflammatory TNFα in response to LPS stimulation and less anti-inflammatory IL-10 and granulocyte colony stimulating factor (G-CSF) than cells from pregnancies with a female fetus, more prostaglandin synthase (PTGS-2) and less prostaglandin dehydrogenase (PGDH). These results suggest that in the presence of a male fetus the trophoblast has the potential to generate a more pro-inflammatory environment. Maturation of the fetal hypothalamic–pituitary–adrenal axis and expression of placental genes, particularly 11β hydroxysteroid dehydrogenase-2 are also expressed in a sex dependent manner, consistent with the sex-biasing influences on gene networks. 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| subjects | 11-beta-Hydroxysteroid Dehydrogenase Type 2 - metabolism Biological and medical sciences Cytokines Embryology: invertebrates and vertebrates. Teratology Female Fetal sex Fetus - physiopathology Fundamental and applied biological sciences. Psychology HPA axis Humans Hypothalamo-Hypophyseal System - physiopathology Infant, Newborn Inflammation Mediators - physiology Internal Medicine Male Obstetric Labor, Premature - etiology Obstetric Labor, Premature - physiopathology Obstetrics and Gynecology Pituitary-Adrenal System - physiopathology Placenta Placenta - physiopathology Pregnancy Pregnancy Complications, Infectious - etiology Pregnancy Complications, Infectious - physiopathology Pregnancy. Parturition. Lactation Premature Birth - etiology Premature Birth - physiopathology Preterm birth Probiotics - therapeutic use Risk Factors Sex Characteristics Stress, Physiological Trophoblasts - physiology Vertebrates: reproduction |
| title | Fetal sex and preterm birth |
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