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Interleukin 10 gene promoter polymorphisms in women with early‐onset pre‐eclampsia
Summary Pre‐eclampsia is one of the most serious disorders of human pregnancy and T helper type 1 (Th1)/Th2 imbalance plays a major role in its aetiology. The Th2 cytokine, interleukin (IL)‐10, plays a significant role in the maintenance of pregnancy. The present study is aimed at understanding the...
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Published in: | Clinical and experimental immunology 2014-11, Vol.178 (2), p.334-341 |
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Pre‐eclampsia is one of the most serious disorders of human pregnancy and T helper type 1 (Th1)/Th2 imbalance plays a major role in its aetiology. The Th2 cytokine, interleukin (IL)‐10, plays a significant role in the maintenance of pregnancy. The present study is aimed at understanding the role of IL‐10 promoter polymorphisms (−1082 G/A; −592 A/C and −819 C/T) and their haplotypes in early‐onset pre‐eclampsia. A total of 120 patients and an equal number of women with normal pregnancy, from Government Maternity Hospital, Petlaburz, Hyderabad, India, were considered for the present study. A standard amplification refractory mutation system–polymerase chain reaction (ARMS–PCR) was carried out for genotyping followed by agarose gel electrophoresis. Appropriate statistical methods were applied to test for the significance of the results. It was found that the IL‐10 −819 C allele (P = 0·003) and −592 A (P = 0·005) allele frequencies increased significantly in patients compared to controls. No significant difference was found with regard to −1082 promoter polymorphism. Haplotype analysis of the IL‐10 single nucleotide polymorphisms (SNPs) revealed a significant association with ACC haplotype with a twofold increased risk in patients compared to controls. The frequencies of two common IL‐10 haplotypes (GCC and ATA) did not show any significant difference. Further, the diplotype analysis revealed five genotypes: −1082A with −819C (P = 0·0016); −1082G with −819C (P = 0·0018); −819C with −592C (P = 0·001); −1082A with −592C (P = 0·032); and −1082G with −592C (P = 0·005) associated with the disease. These findings support the concept of contribution of IL‐10 gene polymorphisms in the pathogenesis of early‐onset pre‐eclampsia. |
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Pre‐eclampsia is one of the most serious disorders of human pregnancy and T helper type 1 (Th1)/Th2 imbalance plays a major role in its aetiology. The Th2 cytokine, interleukin (IL)‐10, plays a significant role in the maintenance of pregnancy. The present study is aimed at understanding the role of IL‐10 promoter polymorphisms (−1082 G/A; −592 A/C and −819 C/T) and their haplotypes in early‐onset pre‐eclampsia. A total of 120 patients and an equal number of women with normal pregnancy, from Government Maternity Hospital, Petlaburz, Hyderabad, India, were considered for the present study. A standard amplification refractory mutation system–polymerase chain reaction (ARMS–PCR) was carried out for genotyping followed by agarose gel electrophoresis. Appropriate statistical methods were applied to test for the significance of the results. It was found that the IL‐10 −819 C allele (P = 0·003) and −592 A (P = 0·005) allele frequencies increased significantly in patients compared to controls. No significant difference was found with regard to −1082 promoter polymorphism. Haplotype analysis of the IL‐10 single nucleotide polymorphisms (SNPs) revealed a significant association with ACC haplotype with a twofold increased risk in patients compared to controls. The frequencies of two common IL‐10 haplotypes (GCC and ATA) did not show any significant difference. Further, the diplotype analysis revealed five genotypes: −1082A with −819C (P = 0·0016); −1082G with −819C (P = 0·0018); −819C with −592C (P = 0·001); −1082A with −592C (P = 0·032); and −1082G with −592C (P = 0·005) associated with the disease. These findings support the concept of contribution of IL‐10 gene polymorphisms in the pathogenesis of early‐onset pre‐eclampsia.</description><identifier>ISSN: 0009-9104</identifier><identifier>EISSN: 1365-2249</identifier><identifier>DOI: 10.1111/cei.12402</identifier><identifier>PMID: 24962617</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>Adult ; Alleles ; Case-Control Studies ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Gestational Age ; haplotype ; Haplotypes ; Humans ; Interleukin-10 - genetics ; interleukin‐10 ; Linkage Disequilibrium ; Odds Ratio ; Original ; Pre-Eclampsia - genetics ; Pregnancy ; pre‐eclampsia ; Promoter Regions, Genetic ; reproductive immunology ; Risk Factors ; Th1/Th2 ; Young Adult</subject><ispartof>Clinical and experimental immunology, 2014-11, Vol.178 (2), p.334-341</ispartof><rights>2014 British Society for Immunology</rights><rights>2014 British Society for Immunology.</rights><rights>Copyright © 2014 British Society for Immunology</rights><rights>2014 British Society for Immunology 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4762-977a5f575667dcc24d8f05e1ff8a4b7e9cc9bfb517f7e56e66d4cef74b29e3c23</citedby><cites>FETCH-LOGICAL-c4762-977a5f575667dcc24d8f05e1ff8a4b7e9cc9bfb517f7e56e66d4cef74b29e3c23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4233382/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4233382/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24962617$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sowmya, S.</creatorcontrib><creatorcontrib>Sri Manjari, K.</creatorcontrib><creatorcontrib>Ramaiah, A.</creatorcontrib><creatorcontrib>Sunitha, T.</creatorcontrib><creatorcontrib>Nallari, P.</creatorcontrib><creatorcontrib>Jyothy, A.</creatorcontrib><creatorcontrib>Venkateshwari, A.</creatorcontrib><title>Interleukin 10 gene promoter polymorphisms in women with early‐onset pre‐eclampsia</title><title>Clinical and experimental immunology</title><addtitle>Clin Exp Immunol</addtitle><description>Summary
Pre‐eclampsia is one of the most serious disorders of human pregnancy and T helper type 1 (Th1)/Th2 imbalance plays a major role in its aetiology. The Th2 cytokine, interleukin (IL)‐10, plays a significant role in the maintenance of pregnancy. The present study is aimed at understanding the role of IL‐10 promoter polymorphisms (−1082 G/A; −592 A/C and −819 C/T) and their haplotypes in early‐onset pre‐eclampsia. A total of 120 patients and an equal number of women with normal pregnancy, from Government Maternity Hospital, Petlaburz, Hyderabad, India, were considered for the present study. A standard amplification refractory mutation system–polymerase chain reaction (ARMS–PCR) was carried out for genotyping followed by agarose gel electrophoresis. Appropriate statistical methods were applied to test for the significance of the results. It was found that the IL‐10 −819 C allele (P = 0·003) and −592 A (P = 0·005) allele frequencies increased significantly in patients compared to controls. No significant difference was found with regard to −1082 promoter polymorphism. Haplotype analysis of the IL‐10 single nucleotide polymorphisms (SNPs) revealed a significant association with ACC haplotype with a twofold increased risk in patients compared to controls. The frequencies of two common IL‐10 haplotypes (GCC and ATA) did not show any significant difference. Further, the diplotype analysis revealed five genotypes: −1082A with −819C (P = 0·0016); −1082G with −819C (P = 0·0018); −819C with −592C (P = 0·001); −1082A with −592C (P = 0·032); and −1082G with −592C (P = 0·005) associated with the disease. These findings support the concept of contribution of IL‐10 gene polymorphisms in the pathogenesis of early‐onset pre‐eclampsia.</description><subject>Adult</subject><subject>Alleles</subject><subject>Case-Control Studies</subject><subject>Female</subject><subject>Gene Frequency</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Gestational Age</subject><subject>haplotype</subject><subject>Haplotypes</subject><subject>Humans</subject><subject>Interleukin-10 - genetics</subject><subject>interleukin‐10</subject><subject>Linkage Disequilibrium</subject><subject>Odds Ratio</subject><subject>Original</subject><subject>Pre-Eclampsia - genetics</subject><subject>Pregnancy</subject><subject>pre‐eclampsia</subject><subject>Promoter Regions, Genetic</subject><subject>reproductive immunology</subject><subject>Risk Factors</subject><subject>Th1/Th2</subject><subject>Young Adult</subject><issn>0009-9104</issn><issn>1365-2249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><recordid>eNqFkcGOFCEQhonRuOPqwRcwnXjRQ-8CTUNzMdlMVp1kEy_qldBMscNKNy10u5mbj-Az-iTWOutGTYyEUAX11R_gJ-QpoycMx6mDcMK4oPweWbFGtjXnQt8nK0qprjWj4og8KuUKt1JK_pAcYVlyydSKfNyMM-QIy6cwVoxWlzBCNeU0JDyuphT3Q8rTLpShVEhcpwFwDfOuApvj_vvXb2ksMGMLYA4u2mEqwT4mD7yNBZ7cxmPy4fX5-_Xb-uLdm8367KJ2Qklea6Vs61vVSqm2znGx7TxtgXnfWdEr0M7p3vctU15BK0HKrXDglei5hsbx5pi8OuhOSz_A1sE4ZxvNlMNg894kG8yflTHszGX6YgRvmqa7EXhxK5DT5wXKbIZQHMRoR0hLMUwynILR5v9o20mqBeMU0ed_oVdpySP-BFLoQae5Eki9PFAup1Iy-Lt7M2pujDVorPlpLLLPfn_oHfnLSQROD8B1iLD_t5JZn28Okj8A-VCvxg</recordid><startdate>201411</startdate><enddate>201411</enddate><creator>Sowmya, S.</creator><creator>Sri Manjari, K.</creator><creator>Ramaiah, A.</creator><creator>Sunitha, T.</creator><creator>Nallari, P.</creator><creator>Jyothy, A.</creator><creator>Venkateshwari, A.</creator><general>Oxford University Press</general><general>Blackwell Science Inc</general><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>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>M7N</scope><scope>7X8</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>201411</creationdate><title>Interleukin 10 gene promoter polymorphisms in women with early‐onset pre‐eclampsia</title><author>Sowmya, S. ; Sri Manjari, K. ; Ramaiah, A. ; Sunitha, T. ; Nallari, P. ; Jyothy, A. ; Venkateshwari, A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4762-977a5f575667dcc24d8f05e1ff8a4b7e9cc9bfb517f7e56e66d4cef74b29e3c23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adult</topic><topic>Alleles</topic><topic>Case-Control Studies</topic><topic>Female</topic><topic>Gene Frequency</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Gestational Age</topic><topic>haplotype</topic><topic>Haplotypes</topic><topic>Humans</topic><topic>Interleukin-10 - genetics</topic><topic>interleukin‐10</topic><topic>Linkage Disequilibrium</topic><topic>Odds Ratio</topic><topic>Original</topic><topic>Pre-Eclampsia - genetics</topic><topic>Pregnancy</topic><topic>pre‐eclampsia</topic><topic>Promoter Regions, Genetic</topic><topic>reproductive immunology</topic><topic>Risk Factors</topic><topic>Th1/Th2</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sowmya, S.</creatorcontrib><creatorcontrib>Sri Manjari, K.</creatorcontrib><creatorcontrib>Ramaiah, A.</creatorcontrib><creatorcontrib>Sunitha, T.</creatorcontrib><creatorcontrib>Nallari, P.</creatorcontrib><creatorcontrib>Jyothy, A.</creatorcontrib><creatorcontrib>Venkateshwari, A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical and experimental immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sowmya, S.</au><au>Sri Manjari, K.</au><au>Ramaiah, A.</au><au>Sunitha, T.</au><au>Nallari, P.</au><au>Jyothy, A.</au><au>Venkateshwari, A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interleukin 10 gene promoter polymorphisms in women with early‐onset pre‐eclampsia</atitle><jtitle>Clinical and experimental immunology</jtitle><addtitle>Clin Exp Immunol</addtitle><date>2014-11</date><risdate>2014</risdate><volume>178</volume><issue>2</issue><spage>334</spage><epage>341</epage><pages>334-341</pages><issn>0009-9104</issn><eissn>1365-2249</eissn><abstract>Summary
Pre‐eclampsia is one of the most serious disorders of human pregnancy and T helper type 1 (Th1)/Th2 imbalance plays a major role in its aetiology. The Th2 cytokine, interleukin (IL)‐10, plays a significant role in the maintenance of pregnancy. The present study is aimed at understanding the role of IL‐10 promoter polymorphisms (−1082 G/A; −592 A/C and −819 C/T) and their haplotypes in early‐onset pre‐eclampsia. A total of 120 patients and an equal number of women with normal pregnancy, from Government Maternity Hospital, Petlaburz, Hyderabad, India, were considered for the present study. A standard amplification refractory mutation system–polymerase chain reaction (ARMS–PCR) was carried out for genotyping followed by agarose gel electrophoresis. Appropriate statistical methods were applied to test for the significance of the results. It was found that the IL‐10 −819 C allele (P = 0·003) and −592 A (P = 0·005) allele frequencies increased significantly in patients compared to controls. No significant difference was found with regard to −1082 promoter polymorphism. Haplotype analysis of the IL‐10 single nucleotide polymorphisms (SNPs) revealed a significant association with ACC haplotype with a twofold increased risk in patients compared to controls. The frequencies of two common IL‐10 haplotypes (GCC and ATA) did not show any significant difference. Further, the diplotype analysis revealed five genotypes: −1082A with −819C (P = 0·0016); −1082G with −819C (P = 0·0018); −819C with −592C (P = 0·001); −1082A with −592C (P = 0·032); and −1082G with −592C (P = 0·005) associated with the disease. These findings support the concept of contribution of IL‐10 gene polymorphisms in the pathogenesis of early‐onset pre‐eclampsia.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>24962617</pmid><doi>10.1111/cei.12402</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult Alleles Case-Control Studies Female Gene Frequency Genetic Predisposition to Disease Genotype Gestational Age haplotype Haplotypes Humans Interleukin-10 - genetics interleukin‐10 Linkage Disequilibrium Odds Ratio Original Pre-Eclampsia - genetics Pregnancy pre‐eclampsia Promoter Regions, Genetic reproductive immunology Risk Factors Th1/Th2 Young Adult |
title | Interleukin 10 gene promoter polymorphisms in women with early‐onset pre‐eclampsia |
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