Association of a maternal CD14 −159 gene polymorphism with preterm premature rupture of membranes and spontaneous preterm birth in multi-fetal pregnancies
CD14, the major receptor for bacterial lipopolysaccharide (LPS) as well as other microbial antigens, is a component of the innate immune system. We hypothesized that a single nucleotide C > T polymorphism at position −159 in the CD14 gene that results in elevated CD14 production would influence s...
Gespeichert in:
| Veröffentlicht in: | Journal of Reproductive Immunology 2006-06, Vol.70 (1), p.109-117 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 117 |
|---|---|
| container_issue | 1 |
| container_start_page | 109 |
| container_title | Journal of Reproductive Immunology |
| container_volume | 70 |
| creator | Kalish, Robin B. Vardhana, Santosh Normand, Neil J. Gupta, Meruka Witkin, Steven S. |
| description | CD14, the major receptor for bacterial lipopolysaccharide (LPS) as well as other microbial antigens, is a component of the innate immune system. We hypothesized that a single nucleotide C
>
T polymorphism at position −159 in the CD14 gene that results in elevated CD14 production would influence susceptibility to preterm premature rupture of membranes (PPROM) and spontaneous preterm birth (SPTB) in multi-fetal pregnancies. DNA from 107 mother–twin and three mother–triplet pairs was analyzed. Pregnancy outcomes were obtained after completion of testing. CD14*T homozygosity was present in 39.3% of 28 women whose pregnancies ended with PPROM, as opposed to 18.1% of 72 pregnancies without a SPTB (
P
=
0.03). There was no relation between the fetal CD14 genotype and PPROM. The likelihood ratio (LR) for PPROM was 2.2 for women homozygous for CD14*T. The LR increased to 3.3 and 3.6 if the CD14 polymorphism was present in combination with previously determined maternal polymorphisms in the genes coding for the inducible 70
kDa heat shock protein (
hsp70-2) and the interleukin-1 receptor antagonist (IL1RN), respectively. Thus, an enhanced maternal pro-inflammatory immune response to LPS may increase susceptibility to PPROM in multi-fetal pregnancies. |
| doi_str_mv | 10.1016/j.jri.2005.12.002 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_67967374</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0165037805001750</els_id><sourcerecordid>67967374</sourcerecordid><originalsourceid>FETCH-LOGICAL-c412t-fe1145b5942572cd7a73adaf5a1fd4d8434282b68ce6bd657f176ad734a8acbb3</originalsourceid><addsrcrecordid>eNqFkc1u1DAUhS0EokPhAdggb2CX4Os4diJW1fArVWIDa8uxndaj2A52AuobsGbN0_VJ6jAjuoPV1ZW_c3x1DkLPgdRAgL8-1IfkakpIWwOtCaEP0A46QSvBSfMQ7QrTVqQR3Rl6kvOBEBCkh8foDDijAhjZod8XOUft1OJiwHHECnu12BTUhPdvgeHbn7-g7fGVDRbPcbrxMc3XLnv8wy3XeE62wH6bRbYmi9M6_5nFyls_JBVsxioYnOcYlrLFNf-VDS4VExewX6fFVaNdyrfl8SqooJ3NT9GjUU3ZPjvNc_T1_bsv-4_V5ecPn_YXl5VmQJeiA2Dt0PaMtoJqI5RolFFjq2A0zHSsYbSjA--05YPhrRhBcGVEw1Sn9DA05-jV0XdO8dtq8yK9y9pO0_FeyUXPRSPYf0EQ0LGSfQHhCOoUc052lHNyXqUbCURu3cmDLN3JrTsJVJbuiubFyXwdvDX3ilNZBXh5AlTWahrTllK-54QQjPTblW-OnC2ZfXc2yVzSDNoal6xepInuH2fcAWLyuso</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>17184603</pqid></control><display><type>article</type><title>Association of a maternal CD14 −159 gene polymorphism with preterm premature rupture of membranes and spontaneous preterm birth in multi-fetal pregnancies</title><source>Wiley Online Library - AutoHoldings Journals</source><source>MEDLINE</source><source>IngentaConnect Free/Open Access Journals</source><source>Access via ScienceDirect (Elsevier)</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Wiley Online Library (Open Access Collection)</source><source>PubMed Central</source><creator>Kalish, Robin B. ; Vardhana, Santosh ; Normand, Neil J. ; Gupta, Meruka ; Witkin, Steven S.</creator><creatorcontrib>Kalish, Robin B. ; Vardhana, Santosh ; Normand, Neil J. ; Gupta, Meruka ; Witkin, Steven S.</creatorcontrib><description>CD14, the major receptor for bacterial lipopolysaccharide (LPS) as well as other microbial antigens, is a component of the innate immune system. We hypothesized that a single nucleotide C
>
T polymorphism at position −159 in the CD14 gene that results in elevated CD14 production would influence susceptibility to preterm premature rupture of membranes (PPROM) and spontaneous preterm birth (SPTB) in multi-fetal pregnancies. DNA from 107 mother–twin and three mother–triplet pairs was analyzed. Pregnancy outcomes were obtained after completion of testing. CD14*T homozygosity was present in 39.3% of 28 women whose pregnancies ended with PPROM, as opposed to 18.1% of 72 pregnancies without a SPTB (
P
=
0.03). There was no relation between the fetal CD14 genotype and PPROM. The likelihood ratio (LR) for PPROM was 2.2 for women homozygous for CD14*T. The LR increased to 3.3 and 3.6 if the CD14 polymorphism was present in combination with previously determined maternal polymorphisms in the genes coding for the inducible 70
kDa heat shock protein (
hsp70-2) and the interleukin-1 receptor antagonist (IL1RN), respectively. Thus, an enhanced maternal pro-inflammatory immune response to LPS may increase susceptibility to PPROM in multi-fetal pregnancies.</description><identifier>ISSN: 0165-0378</identifier><identifier>EISSN: 1872-7603</identifier><identifier>EISSN: 1365-2567</identifier><identifier>DOI: 10.1016/j.jri.2005.12.002</identifier><identifier>PMID: 16427140</identifier><identifier>CODEN: JRIMDR</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>70 kDa heat shock protein ; Biological and medical sciences ; CD14 ; Diseases of mother, fetus and pregnancy ; Female ; Fetal Membranes, Premature Rupture - genetics ; Genetic polymorphism ; Genetic Predisposition to Disease ; Gynecology. Andrology. Obstetrics ; Humans ; Interleukin 1 Receptor Antagonist Protein ; Interleukin-1 receptor antagonist ; Lipopolysaccharide Receptors - genetics ; Medical sciences ; Multi-fetal pregnancies ; Polymorphism, Genetic ; PPROM ; Pregnancy ; Pregnancy, Multiple - genetics ; Pregnancy. Fetus. Placenta ; Premature Birth - genetics ; Sialoglycoproteins - genetics</subject><ispartof>Journal of Reproductive Immunology, 2006-06, Vol.70 (1), p.109-117</ispartof><rights>2005 Elsevier Ireland Ltd</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-fe1145b5942572cd7a73adaf5a1fd4d8434282b68ce6bd657f176ad734a8acbb3</citedby><cites>FETCH-LOGICAL-c412t-fe1145b5942572cd7a73adaf5a1fd4d8434282b68ce6bd657f176ad734a8acbb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jri.2005.12.002$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17774094$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16427140$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kalish, Robin B.</creatorcontrib><creatorcontrib>Vardhana, Santosh</creatorcontrib><creatorcontrib>Normand, Neil J.</creatorcontrib><creatorcontrib>Gupta, Meruka</creatorcontrib><creatorcontrib>Witkin, Steven S.</creatorcontrib><title>Association of a maternal CD14 −159 gene polymorphism with preterm premature rupture of membranes and spontaneous preterm birth in multi-fetal pregnancies</title><title>Journal of Reproductive Immunology</title><addtitle>J Reprod Immunol</addtitle><description>CD14, the major receptor for bacterial lipopolysaccharide (LPS) as well as other microbial antigens, is a component of the innate immune system. We hypothesized that a single nucleotide C
>
T polymorphism at position −159 in the CD14 gene that results in elevated CD14 production would influence susceptibility to preterm premature rupture of membranes (PPROM) and spontaneous preterm birth (SPTB) in multi-fetal pregnancies. DNA from 107 mother–twin and three mother–triplet pairs was analyzed. Pregnancy outcomes were obtained after completion of testing. CD14*T homozygosity was present in 39.3% of 28 women whose pregnancies ended with PPROM, as opposed to 18.1% of 72 pregnancies without a SPTB (
P
=
0.03). There was no relation between the fetal CD14 genotype and PPROM. The likelihood ratio (LR) for PPROM was 2.2 for women homozygous for CD14*T. The LR increased to 3.3 and 3.6 if the CD14 polymorphism was present in combination with previously determined maternal polymorphisms in the genes coding for the inducible 70
kDa heat shock protein (
hsp70-2) and the interleukin-1 receptor antagonist (IL1RN), respectively. Thus, an enhanced maternal pro-inflammatory immune response to LPS may increase susceptibility to PPROM in multi-fetal pregnancies.</description><subject>70 kDa heat shock protein</subject><subject>Biological and medical sciences</subject><subject>CD14</subject><subject>Diseases of mother, fetus and pregnancy</subject><subject>Female</subject><subject>Fetal Membranes, Premature Rupture - genetics</subject><subject>Genetic polymorphism</subject><subject>Genetic Predisposition to Disease</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Interleukin 1 Receptor Antagonist Protein</subject><subject>Interleukin-1 receptor antagonist</subject><subject>Lipopolysaccharide Receptors - genetics</subject><subject>Medical sciences</subject><subject>Multi-fetal pregnancies</subject><subject>Polymorphism, Genetic</subject><subject>PPROM</subject><subject>Pregnancy</subject><subject>Pregnancy, Multiple - genetics</subject><subject>Pregnancy. Fetus. Placenta</subject><subject>Premature Birth - genetics</subject><subject>Sialoglycoproteins - genetics</subject><issn>0165-0378</issn><issn>1872-7603</issn><issn>1365-2567</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1u1DAUhS0EokPhAdggb2CX4Os4diJW1fArVWIDa8uxndaj2A52AuobsGbN0_VJ6jAjuoPV1ZW_c3x1DkLPgdRAgL8-1IfkakpIWwOtCaEP0A46QSvBSfMQ7QrTVqQR3Rl6kvOBEBCkh8foDDijAhjZod8XOUft1OJiwHHECnu12BTUhPdvgeHbn7-g7fGVDRbPcbrxMc3XLnv8wy3XeE62wH6bRbYmi9M6_5nFyls_JBVsxioYnOcYlrLFNf-VDS4VExewX6fFVaNdyrfl8SqooJ3NT9GjUU3ZPjvNc_T1_bsv-4_V5ecPn_YXl5VmQJeiA2Dt0PaMtoJqI5RolFFjq2A0zHSsYbSjA--05YPhrRhBcGVEw1Sn9DA05-jV0XdO8dtq8yK9y9pO0_FeyUXPRSPYf0EQ0LGSfQHhCOoUc052lHNyXqUbCURu3cmDLN3JrTsJVJbuiubFyXwdvDX3ilNZBXh5AlTWahrTllK-54QQjPTblW-OnC2ZfXc2yVzSDNoal6xepInuH2fcAWLyuso</recordid><startdate>20060601</startdate><enddate>20060601</enddate><creator>Kalish, Robin B.</creator><creator>Vardhana, Santosh</creator><creator>Normand, Neil J.</creator><creator>Gupta, Meruka</creator><creator>Witkin, Steven S.</creator><general>Elsevier Ireland Ltd</general><general>Elsevier Science</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>7QL</scope><scope>7T5</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20060601</creationdate><title>Association of a maternal CD14 −159 gene polymorphism with preterm premature rupture of membranes and spontaneous preterm birth in multi-fetal pregnancies</title><author>Kalish, Robin B. ; Vardhana, Santosh ; Normand, Neil J. ; Gupta, Meruka ; Witkin, Steven S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-fe1145b5942572cd7a73adaf5a1fd4d8434282b68ce6bd657f176ad734a8acbb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>70 kDa heat shock protein</topic><topic>Biological and medical sciences</topic><topic>CD14</topic><topic>Diseases of mother, fetus and pregnancy</topic><topic>Female</topic><topic>Fetal Membranes, Premature Rupture - genetics</topic><topic>Genetic polymorphism</topic><topic>Genetic Predisposition to Disease</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Interleukin 1 Receptor Antagonist Protein</topic><topic>Interleukin-1 receptor antagonist</topic><topic>Lipopolysaccharide Receptors - genetics</topic><topic>Medical sciences</topic><topic>Multi-fetal pregnancies</topic><topic>Polymorphism, Genetic</topic><topic>PPROM</topic><topic>Pregnancy</topic><topic>Pregnancy, Multiple - genetics</topic><topic>Pregnancy. Fetus. Placenta</topic><topic>Premature Birth - genetics</topic><topic>Sialoglycoproteins - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kalish, Robin B.</creatorcontrib><creatorcontrib>Vardhana, Santosh</creatorcontrib><creatorcontrib>Normand, Neil J.</creatorcontrib><creatorcontrib>Gupta, Meruka</creatorcontrib><creatorcontrib>Witkin, Steven S.</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of Reproductive Immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kalish, Robin B.</au><au>Vardhana, Santosh</au><au>Normand, Neil J.</au><au>Gupta, Meruka</au><au>Witkin, Steven S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association of a maternal CD14 −159 gene polymorphism with preterm premature rupture of membranes and spontaneous preterm birth in multi-fetal pregnancies</atitle><jtitle>Journal of Reproductive Immunology</jtitle><addtitle>J Reprod Immunol</addtitle><date>2006-06-01</date><risdate>2006</risdate><volume>70</volume><issue>1</issue><spage>109</spage><epage>117</epage><pages>109-117</pages><issn>0165-0378</issn><eissn>1872-7603</eissn><eissn>1365-2567</eissn><coden>JRIMDR</coden><abstract>CD14, the major receptor for bacterial lipopolysaccharide (LPS) as well as other microbial antigens, is a component of the innate immune system. We hypothesized that a single nucleotide C
>
T polymorphism at position −159 in the CD14 gene that results in elevated CD14 production would influence susceptibility to preterm premature rupture of membranes (PPROM) and spontaneous preterm birth (SPTB) in multi-fetal pregnancies. DNA from 107 mother–twin and three mother–triplet pairs was analyzed. Pregnancy outcomes were obtained after completion of testing. CD14*T homozygosity was present in 39.3% of 28 women whose pregnancies ended with PPROM, as opposed to 18.1% of 72 pregnancies without a SPTB (
P
=
0.03). There was no relation between the fetal CD14 genotype and PPROM. The likelihood ratio (LR) for PPROM was 2.2 for women homozygous for CD14*T. The LR increased to 3.3 and 3.6 if the CD14 polymorphism was present in combination with previously determined maternal polymorphisms in the genes coding for the inducible 70
kDa heat shock protein (
hsp70-2) and the interleukin-1 receptor antagonist (IL1RN), respectively. Thus, an enhanced maternal pro-inflammatory immune response to LPS may increase susceptibility to PPROM in multi-fetal pregnancies.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>16427140</pmid><doi>10.1016/j.jri.2005.12.002</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0165-0378 |
| ispartof | Journal of Reproductive Immunology, 2006-06, Vol.70 (1), p.109-117 |
| issn | 0165-0378 1872-7603 1365-2567 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_67967374 |
| source | Wiley Online Library - AutoHoldings Journals; MEDLINE; IngentaConnect Free/Open Access Journals; Access via ScienceDirect (Elsevier); EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); PubMed Central |
| subjects | 70 kDa heat shock protein Biological and medical sciences CD14 Diseases of mother, fetus and pregnancy Female Fetal Membranes, Premature Rupture - genetics Genetic polymorphism Genetic Predisposition to Disease Gynecology. Andrology. Obstetrics Humans Interleukin 1 Receptor Antagonist Protein Interleukin-1 receptor antagonist Lipopolysaccharide Receptors - genetics Medical sciences Multi-fetal pregnancies Polymorphism, Genetic PPROM Pregnancy Pregnancy, Multiple - genetics Pregnancy. Fetus. Placenta Premature Birth - genetics Sialoglycoproteins - genetics |
| title | Association of a maternal CD14 −159 gene polymorphism with preterm premature rupture of membranes and spontaneous preterm birth in multi-fetal pregnancies |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-02T08%3A14%3A22IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Association%20of%20a%20maternal%20CD14%20%E2%88%92159%20gene%20polymorphism%20with%20preterm%20premature%20rupture%20of%20membranes%20and%20spontaneous%20preterm%20birth%20in%20multi-fetal%20pregnancies&rft.jtitle=Journal%20of%20Reproductive%20Immunology&rft.au=Kalish,%20Robin%20B.&rft.date=2006-06-01&rft.volume=70&rft.issue=1&rft.spage=109&rft.epage=117&rft.pages=109-117&rft.issn=0165-0378&rft.eissn=1872-7603&rft.coden=JRIMDR&rft_id=info:doi/10.1016/j.jri.2005.12.002&rft_dat=%3Cproquest_cross%3E67967374%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=17184603&rft_id=info:pmid/16427140&rft_els_id=S0165037805001750&rfr_iscdi=true |