The effect of Escherichia coli lipopolysaccharide and tumour necrosis factor alpha on ovarian function
Pelvic inflammatory disease and metritis are important causes of infertility in humans and domestic animals. Uterine infection with Escherichia coli in cattle is associated with reduced ovarian follicle growth and decreased estradiol secretion. We hypothesized that this effect could be mediated by t...
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Veröffentlicht in: | American journal of reproductive immunology (1989) 2008-11, Vol.60 (5), p.462-473 |
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container_title | American journal of reproductive immunology (1989) |
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creator | Williams, Erin J Sibley, Kelly Miller, Aleisha N Lane, Elizabeth A Fishwick, John Nash, Deborah M Herath, Shan England, Gary C W Dobson, Hilary Sheldon, I Martin |
description | Pelvic inflammatory disease and metritis are important causes of infertility in humans and domestic animals. Uterine infection with Escherichia coli in cattle is associated with reduced ovarian follicle growth and decreased estradiol secretion. We hypothesized that this effect could be mediated by the bacterial lipopolysaccharide (LPS) or cytokines such as tumour necrosis factor alpha (TNFalpha).
In vitro, bovine ovarian theca and granulosa cells were treated with LPS or TNFalpha and steroid secretion measured. In vivo, the effect of LPS or TNFalpha intrauterine infusion was determined by ovarian ultrasonography and measurement of hormones in cattle.
Lipopolysaccharide reduced granulosa cell estradiol secretion, whilst TNFalpha decreased theca and granulosa cell androstenedione and estradiol production, respectively. In vivo, fewer animals ovulated following intrauterine infusion with LPS or TNFalpha.
Lipopolysaccharide and TNFalpha suppress ovarian cell function, supporting the concept that pelvic inflammatory disease and metritis are detrimental for bovine ovarian health. |
doi_str_mv | 10.1111/j.1600-0897.2008.00645.x |
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In vitro, bovine ovarian theca and granulosa cells were treated with LPS or TNFalpha and steroid secretion measured. In vivo, the effect of LPS or TNFalpha intrauterine infusion was determined by ovarian ultrasonography and measurement of hormones in cattle.
Lipopolysaccharide reduced granulosa cell estradiol secretion, whilst TNFalpha decreased theca and granulosa cell androstenedione and estradiol production, respectively. In vivo, fewer animals ovulated following intrauterine infusion with LPS or TNFalpha.
Lipopolysaccharide and TNFalpha suppress ovarian cell function, supporting the concept that pelvic inflammatory disease and metritis are detrimental for bovine ovarian health.</description><identifier>ISSN: 1046-7408</identifier><identifier>EISSN: 1600-0897</identifier><identifier>DOI: 10.1111/j.1600-0897.2008.00645.x</identifier><identifier>PMID: 19238751</identifier><language>eng</language><publisher>Denmark</publisher><subject>Androstenedione - biosynthesis ; Androstenedione - immunology ; Animals ; Cattle ; Cells, Cultured ; Escherichia coli ; Escherichia coli - immunology ; Escherichia coli Infections - immunology ; Estradiol - biosynthesis ; Estradiol - immunology ; Estrogens - biosynthesis ; Estrogens - immunology ; Female ; Follicle Stimulating Hormone - blood ; Lipopolysaccharides - immunology ; Luteinizing Hormone - blood ; Ovarian Follicle - drug effects ; Ovarian Follicle - immunology ; Ovulation - drug effects ; Ovulation - immunology ; Pelvic Inflammatory Disease - etiology ; Pelvic Inflammatory Disease - immunology ; Tumor Necrosis Factor-alpha - immunology ; Tumor Necrosis Factor-alpha - pharmacology</subject><ispartof>American journal of reproductive immunology (1989), 2008-11, Vol.60 (5), p.462-473</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19238751$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Williams, Erin J</creatorcontrib><creatorcontrib>Sibley, Kelly</creatorcontrib><creatorcontrib>Miller, Aleisha N</creatorcontrib><creatorcontrib>Lane, Elizabeth A</creatorcontrib><creatorcontrib>Fishwick, John</creatorcontrib><creatorcontrib>Nash, Deborah M</creatorcontrib><creatorcontrib>Herath, Shan</creatorcontrib><creatorcontrib>England, Gary C W</creatorcontrib><creatorcontrib>Dobson, Hilary</creatorcontrib><creatorcontrib>Sheldon, I Martin</creatorcontrib><title>The effect of Escherichia coli lipopolysaccharide and tumour necrosis factor alpha on ovarian function</title><title>American journal of reproductive immunology (1989)</title><addtitle>Am J Reprod Immunol</addtitle><description>Pelvic inflammatory disease and metritis are important causes of infertility in humans and domestic animals. Uterine infection with Escherichia coli in cattle is associated with reduced ovarian follicle growth and decreased estradiol secretion. We hypothesized that this effect could be mediated by the bacterial lipopolysaccharide (LPS) or cytokines such as tumour necrosis factor alpha (TNFalpha).
In vitro, bovine ovarian theca and granulosa cells were treated with LPS or TNFalpha and steroid secretion measured. In vivo, the effect of LPS or TNFalpha intrauterine infusion was determined by ovarian ultrasonography and measurement of hormones in cattle.
Lipopolysaccharide reduced granulosa cell estradiol secretion, whilst TNFalpha decreased theca and granulosa cell androstenedione and estradiol production, respectively. In vivo, fewer animals ovulated following intrauterine infusion with LPS or TNFalpha.
Lipopolysaccharide and TNFalpha suppress ovarian cell function, supporting the concept that pelvic inflammatory disease and metritis are detrimental for bovine ovarian health.</description><subject>Androstenedione - biosynthesis</subject><subject>Androstenedione - immunology</subject><subject>Animals</subject><subject>Cattle</subject><subject>Cells, Cultured</subject><subject>Escherichia coli</subject><subject>Escherichia coli - immunology</subject><subject>Escherichia coli Infections - immunology</subject><subject>Estradiol - biosynthesis</subject><subject>Estradiol - immunology</subject><subject>Estrogens - biosynthesis</subject><subject>Estrogens - immunology</subject><subject>Female</subject><subject>Follicle Stimulating Hormone - blood</subject><subject>Lipopolysaccharides - immunology</subject><subject>Luteinizing Hormone - blood</subject><subject>Ovarian Follicle - drug effects</subject><subject>Ovarian Follicle - immunology</subject><subject>Ovulation - drug effects</subject><subject>Ovulation - immunology</subject><subject>Pelvic Inflammatory Disease - etiology</subject><subject>Pelvic Inflammatory Disease - immunology</subject><subject>Tumor Necrosis Factor-alpha - immunology</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><issn>1046-7408</issn><issn>1600-0897</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkN1LwzAUxYMobk7_BcmTb61J0zbJiyBjfsDAl_lc0nzYjC6pSTvcf2_AOfS-3Avn8DucCwDEKMdp7rc5rhHKEOM0LxBiOUJ1WeVfZ2B-Es7Tjco6oyViM3AV4xYlJyf0EswwLwijFZ4Ds-k01MZoOUJv4CrKTgcrOyug9L2FvR384PtDFFJ2IliloXAKjtPOTwE6LYOPNkIj5OgDFP3QCegd9PvkFQ6aycnRencNLozoo7457gV4f1ptli_Z-u35dfm4zoaCV2OmW1qqqjSSGUIMo4YzRSvaqqplrMWUloSkaoJjgVtFKkJ5EjVRLebY6IIswMMPd5janVZSuzGIvhmC3YlwaLywzX_F2a758PumoKhAlCfA3REQ_Oek49jsbJS674XTfooN5jWuywIl4-3fpFPE72vJN5epgEk</recordid><startdate>20081101</startdate><enddate>20081101</enddate><creator>Williams, Erin J</creator><creator>Sibley, Kelly</creator><creator>Miller, Aleisha N</creator><creator>Lane, Elizabeth A</creator><creator>Fishwick, John</creator><creator>Nash, Deborah M</creator><creator>Herath, Shan</creator><creator>England, Gary C W</creator><creator>Dobson, Hilary</creator><creator>Sheldon, I Martin</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QL</scope><scope>7T5</scope><scope>C1K</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>20081101</creationdate><title>The effect of Escherichia coli lipopolysaccharide and tumour necrosis factor alpha on ovarian function</title><author>Williams, Erin J ; Sibley, Kelly ; Miller, Aleisha N ; Lane, Elizabeth A ; Fishwick, John ; Nash, Deborah M ; Herath, Shan ; England, Gary C W ; Dobson, Hilary ; Sheldon, I Martin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p295t-eb74d54fc8f33f87f98d757bd5b88b177433897a91a1bd353797bde3db191fe23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Androstenedione - biosynthesis</topic><topic>Androstenedione - immunology</topic><topic>Animals</topic><topic>Cattle</topic><topic>Cells, Cultured</topic><topic>Escherichia coli</topic><topic>Escherichia coli - immunology</topic><topic>Escherichia coli Infections - immunology</topic><topic>Estradiol - biosynthesis</topic><topic>Estradiol - immunology</topic><topic>Estrogens - biosynthesis</topic><topic>Estrogens - immunology</topic><topic>Female</topic><topic>Follicle Stimulating Hormone - blood</topic><topic>Lipopolysaccharides - immunology</topic><topic>Luteinizing Hormone - blood</topic><topic>Ovarian Follicle - drug effects</topic><topic>Ovarian Follicle - immunology</topic><topic>Ovulation - drug effects</topic><topic>Ovulation - immunology</topic><topic>Pelvic Inflammatory Disease - etiology</topic><topic>Pelvic Inflammatory Disease - immunology</topic><topic>Tumor Necrosis Factor-alpha - immunology</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Williams, Erin J</creatorcontrib><creatorcontrib>Sibley, Kelly</creatorcontrib><creatorcontrib>Miller, Aleisha N</creatorcontrib><creatorcontrib>Lane, Elizabeth A</creatorcontrib><creatorcontrib>Fishwick, John</creatorcontrib><creatorcontrib>Nash, Deborah M</creatorcontrib><creatorcontrib>Herath, Shan</creatorcontrib><creatorcontrib>England, Gary C W</creatorcontrib><creatorcontrib>Dobson, Hilary</creatorcontrib><creatorcontrib>Sheldon, I Martin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of reproductive immunology (1989)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Williams, Erin J</au><au>Sibley, Kelly</au><au>Miller, Aleisha N</au><au>Lane, Elizabeth A</au><au>Fishwick, John</au><au>Nash, Deborah M</au><au>Herath, Shan</au><au>England, Gary C W</au><au>Dobson, Hilary</au><au>Sheldon, I Martin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The effect of Escherichia coli lipopolysaccharide and tumour necrosis factor alpha on ovarian function</atitle><jtitle>American journal of reproductive immunology (1989)</jtitle><addtitle>Am J Reprod Immunol</addtitle><date>2008-11-01</date><risdate>2008</risdate><volume>60</volume><issue>5</issue><spage>462</spage><epage>473</epage><pages>462-473</pages><issn>1046-7408</issn><eissn>1600-0897</eissn><abstract>Pelvic inflammatory disease and metritis are important causes of infertility in humans and domestic animals. Uterine infection with Escherichia coli in cattle is associated with reduced ovarian follicle growth and decreased estradiol secretion. We hypothesized that this effect could be mediated by the bacterial lipopolysaccharide (LPS) or cytokines such as tumour necrosis factor alpha (TNFalpha).
In vitro, bovine ovarian theca and granulosa cells were treated with LPS or TNFalpha and steroid secretion measured. In vivo, the effect of LPS or TNFalpha intrauterine infusion was determined by ovarian ultrasonography and measurement of hormones in cattle.
Lipopolysaccharide reduced granulosa cell estradiol secretion, whilst TNFalpha decreased theca and granulosa cell androstenedione and estradiol production, respectively. In vivo, fewer animals ovulated following intrauterine infusion with LPS or TNFalpha.
Lipopolysaccharide and TNFalpha suppress ovarian cell function, supporting the concept that pelvic inflammatory disease and metritis are detrimental for bovine ovarian health.</abstract><cop>Denmark</cop><pmid>19238751</pmid><doi>10.1111/j.1600-0897.2008.00645.x</doi><tpages>12</tpages></addata></record> |
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subjects | Androstenedione - biosynthesis Androstenedione - immunology Animals Cattle Cells, Cultured Escherichia coli Escherichia coli - immunology Escherichia coli Infections - immunology Estradiol - biosynthesis Estradiol - immunology Estrogens - biosynthesis Estrogens - immunology Female Follicle Stimulating Hormone - blood Lipopolysaccharides - immunology Luteinizing Hormone - blood Ovarian Follicle - drug effects Ovarian Follicle - immunology Ovulation - drug effects Ovulation - immunology Pelvic Inflammatory Disease - etiology Pelvic Inflammatory Disease - immunology Tumor Necrosis Factor-alpha - immunology Tumor Necrosis Factor-alpha - pharmacology |
title | The effect of Escherichia coli lipopolysaccharide and tumour necrosis factor alpha on ovarian function |
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