Polymorphisms of endotoxin pathway and endotoxin exposure: in vitro IgE synthesis and replication in a birth cohort
Background Genetic variants in endotoxin signaling pathway are important in modulating the effect of environmental endotoxin on asthma and atopic phenotypes. Our objective was to determine the single nucleotide polymorphisms (SNPs) in the endotoxin signaling pathway that may influence in vitro IgE s...
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| Veröffentlicht in: | Allergy (Copenhagen) 2014-12, Vol.69 (12), p.1648-1658 |
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| creator | Sahiner, U. M. Semic‐Jusufagic, A. Curtin, J. A. Birben, E. Belgrave, D. Sackesen, C. Simpson, A. Yavuz, T. S. Akdis, C. A. Custovic, A. Kalayci, O. |
| description | Background
Genetic variants in endotoxin signaling pathway are important in modulating the effect of environmental endotoxin on asthma and atopic phenotypes. Our objective was to determine the single nucleotide polymorphisms (SNPs) in the endotoxin signaling pathway that may influence in vitro IgE synthesis and to investigate the relationship between these variants and endotoxin exposure in relation to the development of asthma and atopy in a birth cohort.
Methods
Peripheral blood mononuclear cells from 45 children with asthma were stimulated with 2 and 200 ng/ml lipopolysaccharide in vitro and IgE was measured in the culture supernatants. Children were genotyped for 121 SNPs from 30 genes in the endotoxin signaling pathway. Variants with a dose–response IgE production in relation to lipopolysaccharide (LPS) were selected for replication in a population‐based birth cohort, in which we investigated the interaction between these SNPs and endotoxin exposure in relation to airway hyper‐responsiveness, wheeze, and atopic sensitization.
Results
Twenty‐one SNPs in nine genes (CD14, TLR4, IRF3, TRAF‐6, TIRAP, TRIF, IKK‐1, ST‐2, SOCS1) were found to modulate the effect of endotoxin on in vitro IgE synthesis, with six displaying high linkage disequilibrium. Of the remaining 15 SNPs, for seven we found significant relationships between genotype and endotoxin exposure in the genetic association study in relation to symptomatic airway hyper‐responsiveness (CD14‐rs2915863 and rs2569191, TRIF‐rs4807000), current wheeze (ST‐2‐rs17639215, IKK‐1‐rs2230804, and TRIF‐rs4807000), and atopy (CD14‐rs2915863 and rs2569192, TRAF‐6‐rs5030411, and IKK‐1‐rs2230804).
Conclusions
Variants in the endotoxin signaling pathway are important determinants of asthma and atopy. The genotype effect is a function of the environmental endotoxin exposure. |
| doi_str_mv | 10.1111/all.12504 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1635037638</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1635037638</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3864-494de43701a73c6f0465a66aee9f9b3bec1fea5e8151d958048347a0ea910ba13</originalsourceid><addsrcrecordid>eNp10cFO3DAQBmALtYJl2wMvgCz1Qg_ZHcd2EnNDKwpIK7WH9hw5yYQYJXGwE9i8PWYXUFWpvlgeffpl_UPIGYMVC2et23bFYgniiCwYV1mklJKfyAIYyEhInp2QU-8fACCNFRyTk1gyiNNELIj_Zdu5s25ojO88tTXFvrKj3ZmeDnpsnvVMdV_9NcXdYP3k8JKGx5MZnaV399fUz_3YoDd-zx0OrSn1aGz_yjQtjBsbWtrGuvEL-Vzr1uPXt3tJ_vy4_r25jbY_b-42V9uo5FkiIqFEhYKnwHTKy6QGkUidJBpR1argBZasRi0xY5JVSmYgMi5SDagVg0IzviQXh9zB2ccJ_Zh3xpfYtrpHO_mcJVwCTxOeBfrtH_pgJ9eH3wUVh44h9BrU94MqnfXeYZ0PznTazTmD_HUTedhEvt9EsOdviVPRYfUh36sPYH0Az6bF-f9J-dV2e4h8AR2Rkvw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1621110139</pqid></control><display><type>article</type><title>Polymorphisms of endotoxin pathway and endotoxin exposure: in vitro IgE synthesis and replication in a birth cohort</title><source>Wiley Free Content</source><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Sahiner, U. M. ; Semic‐Jusufagic, A. ; Curtin, J. A. ; Birben, E. ; Belgrave, D. ; Sackesen, C. ; Simpson, A. ; Yavuz, T. S. ; Akdis, C. A. ; Custovic, A. ; Kalayci, O.</creator><creatorcontrib>Sahiner, U. M. ; Semic‐Jusufagic, A. ; Curtin, J. A. ; Birben, E. ; Belgrave, D. ; Sackesen, C. ; Simpson, A. ; Yavuz, T. S. ; Akdis, C. A. ; Custovic, A. ; Kalayci, O.</creatorcontrib><description>Background
Genetic variants in endotoxin signaling pathway are important in modulating the effect of environmental endotoxin on asthma and atopic phenotypes. Our objective was to determine the single nucleotide polymorphisms (SNPs) in the endotoxin signaling pathway that may influence in vitro IgE synthesis and to investigate the relationship between these variants and endotoxin exposure in relation to the development of asthma and atopy in a birth cohort.
Methods
Peripheral blood mononuclear cells from 45 children with asthma were stimulated with 2 and 200 ng/ml lipopolysaccharide in vitro and IgE was measured in the culture supernatants. Children were genotyped for 121 SNPs from 30 genes in the endotoxin signaling pathway. Variants with a dose–response IgE production in relation to lipopolysaccharide (LPS) were selected for replication in a population‐based birth cohort, in which we investigated the interaction between these SNPs and endotoxin exposure in relation to airway hyper‐responsiveness, wheeze, and atopic sensitization.
Results
Twenty‐one SNPs in nine genes (CD14, TLR4, IRF3, TRAF‐6, TIRAP, TRIF, IKK‐1, ST‐2, SOCS1) were found to modulate the effect of endotoxin on in vitro IgE synthesis, with six displaying high linkage disequilibrium. Of the remaining 15 SNPs, for seven we found significant relationships between genotype and endotoxin exposure in the genetic association study in relation to symptomatic airway hyper‐responsiveness (CD14‐rs2915863 and rs2569191, TRIF‐rs4807000), current wheeze (ST‐2‐rs17639215, IKK‐1‐rs2230804, and TRIF‐rs4807000), and atopy (CD14‐rs2915863 and rs2569192, TRAF‐6‐rs5030411, and IKK‐1‐rs2230804).
Conclusions
Variants in the endotoxin signaling pathway are important determinants of asthma and atopy. The genotype effect is a function of the environmental endotoxin exposure.</description><identifier>ISSN: 0105-4538</identifier><identifier>EISSN: 1398-9995</identifier><identifier>DOI: 10.1111/all.12504</identifier><identifier>PMID: 25102764</identifier><language>eng</language><publisher>Denmark: Blackwell Publishing Ltd</publisher><subject>Adolescent ; Alleles ; Asthma ; Asthma - diagnosis ; Asthma - genetics ; Asthma - immunology ; atopy ; Cells, Cultured ; Child ; Cohort Studies ; endotoxin ; Endotoxins - immunology ; Endotoxins - metabolism ; Environmental Exposure ; gene ; Genetic Association Studies ; Genetic Predisposition to Disease ; Genotype ; Genotype & phenotype ; Humans ; Hypersensitivity, Immediate - diagnosis ; Hypersensitivity, Immediate - genetics ; Hypersensitivity, Immediate - immunology ; IgE ; Immunoglobulin E - biosynthesis ; Immunoglobulin E - immunology ; In Vitro Techniques ; Leukocytes, Mononuclear - immunology ; Leukocytes, Mononuclear - metabolism ; Polymorphism ; Polymorphism, Genetic ; Polymorphism, Single Nucleotide ; Signal Transduction</subject><ispartof>Allergy (Copenhagen), 2014-12, Vol.69 (12), p.1648-1658</ispartof><rights>2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</rights><rights>2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.</rights><rights>Copyright © 2014 John Wiley & Sons A/S</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3864-494de43701a73c6f0465a66aee9f9b3bec1fea5e8151d958048347a0ea910ba13</citedby><cites>FETCH-LOGICAL-c3864-494de43701a73c6f0465a66aee9f9b3bec1fea5e8151d958048347a0ea910ba13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fall.12504$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fall.12504$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25102764$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sahiner, U. M.</creatorcontrib><creatorcontrib>Semic‐Jusufagic, A.</creatorcontrib><creatorcontrib>Curtin, J. A.</creatorcontrib><creatorcontrib>Birben, E.</creatorcontrib><creatorcontrib>Belgrave, D.</creatorcontrib><creatorcontrib>Sackesen, C.</creatorcontrib><creatorcontrib>Simpson, A.</creatorcontrib><creatorcontrib>Yavuz, T. S.</creatorcontrib><creatorcontrib>Akdis, C. A.</creatorcontrib><creatorcontrib>Custovic, A.</creatorcontrib><creatorcontrib>Kalayci, O.</creatorcontrib><title>Polymorphisms of endotoxin pathway and endotoxin exposure: in vitro IgE synthesis and replication in a birth cohort</title><title>Allergy (Copenhagen)</title><addtitle>Allergy</addtitle><description>Background
Genetic variants in endotoxin signaling pathway are important in modulating the effect of environmental endotoxin on asthma and atopic phenotypes. Our objective was to determine the single nucleotide polymorphisms (SNPs) in the endotoxin signaling pathway that may influence in vitro IgE synthesis and to investigate the relationship between these variants and endotoxin exposure in relation to the development of asthma and atopy in a birth cohort.
Methods
Peripheral blood mononuclear cells from 45 children with asthma were stimulated with 2 and 200 ng/ml lipopolysaccharide in vitro and IgE was measured in the culture supernatants. Children were genotyped for 121 SNPs from 30 genes in the endotoxin signaling pathway. Variants with a dose–response IgE production in relation to lipopolysaccharide (LPS) were selected for replication in a population‐based birth cohort, in which we investigated the interaction between these SNPs and endotoxin exposure in relation to airway hyper‐responsiveness, wheeze, and atopic sensitization.
Results
Twenty‐one SNPs in nine genes (CD14, TLR4, IRF3, TRAF‐6, TIRAP, TRIF, IKK‐1, ST‐2, SOCS1) were found to modulate the effect of endotoxin on in vitro IgE synthesis, with six displaying high linkage disequilibrium. Of the remaining 15 SNPs, for seven we found significant relationships between genotype and endotoxin exposure in the genetic association study in relation to symptomatic airway hyper‐responsiveness (CD14‐rs2915863 and rs2569191, TRIF‐rs4807000), current wheeze (ST‐2‐rs17639215, IKK‐1‐rs2230804, and TRIF‐rs4807000), and atopy (CD14‐rs2915863 and rs2569192, TRAF‐6‐rs5030411, and IKK‐1‐rs2230804).
Conclusions
Variants in the endotoxin signaling pathway are important determinants of asthma and atopy. The genotype effect is a function of the environmental endotoxin exposure.</description><subject>Adolescent</subject><subject>Alleles</subject><subject>Asthma</subject><subject>Asthma - diagnosis</subject><subject>Asthma - genetics</subject><subject>Asthma - immunology</subject><subject>atopy</subject><subject>Cells, Cultured</subject><subject>Child</subject><subject>Cohort Studies</subject><subject>endotoxin</subject><subject>Endotoxins - immunology</subject><subject>Endotoxins - metabolism</subject><subject>Environmental Exposure</subject><subject>gene</subject><subject>Genetic Association Studies</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Genotype & phenotype</subject><subject>Humans</subject><subject>Hypersensitivity, Immediate - diagnosis</subject><subject>Hypersensitivity, Immediate - genetics</subject><subject>Hypersensitivity, Immediate - immunology</subject><subject>IgE</subject><subject>Immunoglobulin E - biosynthesis</subject><subject>Immunoglobulin E - immunology</subject><subject>In Vitro Techniques</subject><subject>Leukocytes, Mononuclear - immunology</subject><subject>Leukocytes, Mononuclear - metabolism</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Signal Transduction</subject><issn>0105-4538</issn><issn>1398-9995</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10cFO3DAQBmALtYJl2wMvgCz1Qg_ZHcd2EnNDKwpIK7WH9hw5yYQYJXGwE9i8PWYXUFWpvlgeffpl_UPIGYMVC2et23bFYgniiCwYV1mklJKfyAIYyEhInp2QU-8fACCNFRyTk1gyiNNELIj_Zdu5s25ojO88tTXFvrKj3ZmeDnpsnvVMdV_9NcXdYP3k8JKGx5MZnaV399fUz_3YoDd-zx0OrSn1aGz_yjQtjBsbWtrGuvEL-Vzr1uPXt3tJ_vy4_r25jbY_b-42V9uo5FkiIqFEhYKnwHTKy6QGkUidJBpR1argBZasRi0xY5JVSmYgMi5SDagVg0IzviQXh9zB2ccJ_Zh3xpfYtrpHO_mcJVwCTxOeBfrtH_pgJ9eH3wUVh44h9BrU94MqnfXeYZ0PznTazTmD_HUTedhEvt9EsOdviVPRYfUh36sPYH0Az6bF-f9J-dV2e4h8AR2Rkvw</recordid><startdate>201412</startdate><enddate>201412</enddate><creator>Sahiner, U. M.</creator><creator>Semic‐Jusufagic, A.</creator><creator>Curtin, J. A.</creator><creator>Birben, E.</creator><creator>Belgrave, D.</creator><creator>Sackesen, C.</creator><creator>Simpson, A.</creator><creator>Yavuz, T. S.</creator><creator>Akdis, C. A.</creator><creator>Custovic, A.</creator><creator>Kalayci, O.</creator><general>Blackwell Publishing Ltd</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>H94</scope><scope>K9.</scope><scope>7T7</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope></search><sort><creationdate>201412</creationdate><title>Polymorphisms of endotoxin pathway and endotoxin exposure: in vitro IgE synthesis and replication in a birth cohort</title><author>Sahiner, U. M. ; Semic‐Jusufagic, A. ; Curtin, J. A. ; Birben, E. ; Belgrave, D. ; Sackesen, C. ; Simpson, A. ; Yavuz, T. S. ; Akdis, C. A. ; Custovic, A. ; Kalayci, O.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3864-494de43701a73c6f0465a66aee9f9b3bec1fea5e8151d958048347a0ea910ba13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adolescent</topic><topic>Alleles</topic><topic>Asthma</topic><topic>Asthma - diagnosis</topic><topic>Asthma - genetics</topic><topic>Asthma - immunology</topic><topic>atopy</topic><topic>Cells, Cultured</topic><topic>Child</topic><topic>Cohort Studies</topic><topic>endotoxin</topic><topic>Endotoxins - immunology</topic><topic>Endotoxins - metabolism</topic><topic>Environmental Exposure</topic><topic>gene</topic><topic>Genetic Association Studies</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Genotype & phenotype</topic><topic>Humans</topic><topic>Hypersensitivity, Immediate - diagnosis</topic><topic>Hypersensitivity, Immediate - genetics</topic><topic>Hypersensitivity, Immediate - immunology</topic><topic>IgE</topic><topic>Immunoglobulin E - biosynthesis</topic><topic>Immunoglobulin E - immunology</topic><topic>In Vitro Techniques</topic><topic>Leukocytes, Mononuclear - immunology</topic><topic>Leukocytes, Mononuclear - metabolism</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sahiner, U. M.</creatorcontrib><creatorcontrib>Semic‐Jusufagic, A.</creatorcontrib><creatorcontrib>Curtin, J. A.</creatorcontrib><creatorcontrib>Birben, E.</creatorcontrib><creatorcontrib>Belgrave, D.</creatorcontrib><creatorcontrib>Sackesen, C.</creatorcontrib><creatorcontrib>Simpson, A.</creatorcontrib><creatorcontrib>Yavuz, T. S.</creatorcontrib><creatorcontrib>Akdis, C. A.</creatorcontrib><creatorcontrib>Custovic, A.</creatorcontrib><creatorcontrib>Kalayci, O.</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>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Allergy (Copenhagen)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sahiner, U. M.</au><au>Semic‐Jusufagic, A.</au><au>Curtin, J. A.</au><au>Birben, E.</au><au>Belgrave, D.</au><au>Sackesen, C.</au><au>Simpson, A.</au><au>Yavuz, T. S.</au><au>Akdis, C. A.</au><au>Custovic, A.</au><au>Kalayci, O.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Polymorphisms of endotoxin pathway and endotoxin exposure: in vitro IgE synthesis and replication in a birth cohort</atitle><jtitle>Allergy (Copenhagen)</jtitle><addtitle>Allergy</addtitle><date>2014-12</date><risdate>2014</risdate><volume>69</volume><issue>12</issue><spage>1648</spage><epage>1658</epage><pages>1648-1658</pages><issn>0105-4538</issn><eissn>1398-9995</eissn><abstract>Background
Genetic variants in endotoxin signaling pathway are important in modulating the effect of environmental endotoxin on asthma and atopic phenotypes. Our objective was to determine the single nucleotide polymorphisms (SNPs) in the endotoxin signaling pathway that may influence in vitro IgE synthesis and to investigate the relationship between these variants and endotoxin exposure in relation to the development of asthma and atopy in a birth cohort.
Methods
Peripheral blood mononuclear cells from 45 children with asthma were stimulated with 2 and 200 ng/ml lipopolysaccharide in vitro and IgE was measured in the culture supernatants. Children were genotyped for 121 SNPs from 30 genes in the endotoxin signaling pathway. Variants with a dose–response IgE production in relation to lipopolysaccharide (LPS) were selected for replication in a population‐based birth cohort, in which we investigated the interaction between these SNPs and endotoxin exposure in relation to airway hyper‐responsiveness, wheeze, and atopic sensitization.
Results
Twenty‐one SNPs in nine genes (CD14, TLR4, IRF3, TRAF‐6, TIRAP, TRIF, IKK‐1, ST‐2, SOCS1) were found to modulate the effect of endotoxin on in vitro IgE synthesis, with six displaying high linkage disequilibrium. Of the remaining 15 SNPs, for seven we found significant relationships between genotype and endotoxin exposure in the genetic association study in relation to symptomatic airway hyper‐responsiveness (CD14‐rs2915863 and rs2569191, TRIF‐rs4807000), current wheeze (ST‐2‐rs17639215, IKK‐1‐rs2230804, and TRIF‐rs4807000), and atopy (CD14‐rs2915863 and rs2569192, TRAF‐6‐rs5030411, and IKK‐1‐rs2230804).
Conclusions
Variants in the endotoxin signaling pathway are important determinants of asthma and atopy. The genotype effect is a function of the environmental endotoxin exposure.</abstract><cop>Denmark</cop><pub>Blackwell Publishing Ltd</pub><pmid>25102764</pmid><doi>10.1111/all.12504</doi><tpages>11</tpages></addata></record> |
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| source | Wiley Free Content; MEDLINE; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Adolescent Alleles Asthma Asthma - diagnosis Asthma - genetics Asthma - immunology atopy Cells, Cultured Child Cohort Studies endotoxin Endotoxins - immunology Endotoxins - metabolism Environmental Exposure gene Genetic Association Studies Genetic Predisposition to Disease Genotype Genotype & phenotype Humans Hypersensitivity, Immediate - diagnosis Hypersensitivity, Immediate - genetics Hypersensitivity, Immediate - immunology IgE Immunoglobulin E - biosynthesis Immunoglobulin E - immunology In Vitro Techniques Leukocytes, Mononuclear - immunology Leukocytes, Mononuclear - metabolism Polymorphism Polymorphism, Genetic Polymorphism, Single Nucleotide Signal Transduction |
| title | Polymorphisms of endotoxin pathway and endotoxin exposure: in vitro IgE synthesis and replication in a birth cohort |
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