Mannose‐binding lectin 2 (MBL2) gene polymorphism in asthma and atopy among adults
Summary Mannose‐binding lectin (MBL) insufficiency due to polymorphisms in the MBL2 gene causes an opsonization defect, which has been connected to infections and atopy. We investigated the significance of MBL2 genotypes with regard to persistent asthma and atopy among adults. The genotypes were det...
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Veröffentlicht in: | Clinical and experimental immunology 2005-10, Vol.142 (1), p.120-124 |
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description | Summary
Mannose‐binding lectin (MBL) insufficiency due to polymorphisms in the MBL2 gene causes an opsonization defect, which has been connected to infections and atopy. We investigated the significance of MBL2 genotypes with regard to persistent asthma and atopy among adults. The genotypes were determined in 243 adults with persistent asthma and 400 controls. Atopy was determined by skin‐prick test. As a result, the carriage of −221 base pairs (bp) promoter region variant allele X (nucleotide change G→C; alleles Y→X, respectively) causing low MBL expression proved to be a significant risk factor for asthma in non‐atopic males [odds ratio (OR) = 2·52, 95% confidence interval (CI) = 1·23–5·15; P = 0·01]. Furthermore, the X‐allele carriage was associated with the decrease in lung function (forced expiratory volume at 1 s, FEV1) during follow‐up in the patients with asthma (P = 0·033), the effect being strongest for non‐atopic asthmatics (P = 0·042). The MBL2 genotype had no clear effect on the occurrence of atopy in adults. In conclusion, our results abrogate the previously suggested predisposing effect of MBL insufficiency on atopy at least in adults. However, as MBL is a complement component participating in immune defence against microbes, and as in the pathogenesis of non‐atopic asthma infectious agents are probably involved, the gene–environment interactions between MBL and infections should be assessed further with regard to asthma. |
doi_str_mv | 10.1111/j.1365-2249.2005.02881.x |
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Mannose‐binding lectin (MBL) insufficiency due to polymorphisms in the MBL2 gene causes an opsonization defect, which has been connected to infections and atopy. We investigated the significance of MBL2 genotypes with regard to persistent asthma and atopy among adults. The genotypes were determined in 243 adults with persistent asthma and 400 controls. Atopy was determined by skin‐prick test. As a result, the carriage of −221 base pairs (bp) promoter region variant allele X (nucleotide change G→C; alleles Y→X, respectively) causing low MBL expression proved to be a significant risk factor for asthma in non‐atopic males [odds ratio (OR) = 2·52, 95% confidence interval (CI) = 1·23–5·15; P = 0·01]. Furthermore, the X‐allele carriage was associated with the decrease in lung function (forced expiratory volume at 1 s, FEV1) during follow‐up in the patients with asthma (P = 0·033), the effect being strongest for non‐atopic asthmatics (P = 0·042). The MBL2 genotype had no clear effect on the occurrence of atopy in adults. In conclusion, our results abrogate the previously suggested predisposing effect of MBL insufficiency on atopy at least in adults. However, as MBL is a complement component participating in immune defence against microbes, and as in the pathogenesis of non‐atopic asthma infectious agents are probably involved, the gene–environment interactions between MBL and infections should be assessed further with regard to asthma.</description><identifier>ISSN: 0009-9104</identifier><identifier>EISSN: 1365-2249</identifier><identifier>DOI: 10.1111/j.1365-2249.2005.02881.x</identifier><identifier>PMID: 16178865</identifier><identifier>CODEN: CEXIAL</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Adult ; Aged ; Aged, 80 and over ; asthma ; Asthma - immunology ; Asthma - physiopathology ; atopy ; Biological and medical sciences ; Female ; Forced Expiratory Volume - physiology ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Genetic Predisposition to Disease - genetics ; Genotype ; Humans ; Immunopathology ; Male ; Mannose-Binding Lectin - genetics ; mannose‐binding lectin ; Medical sciences ; Middle Aged ; Original ; Polymorphism, Genetic - genetics ; Promoter Regions, Genetic - genetics</subject><ispartof>Clinical and experimental immunology, 2005-10, Vol.142 (1), p.120-124</ispartof><rights>2005 INIST-CNRS</rights><rights>Copyright Blackwell Publishing Oct 2005</rights><rights>2005 British Society for Immunology 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5291-e6d2ce702ae419b0b7f166a749645afa0ed76546e8fecfbc0b4c4a168c9239d43</citedby><cites>FETCH-LOGICAL-c5291-e6d2ce702ae419b0b7f166a749645afa0ed76546e8fecfbc0b4c4a168c9239d43</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/PMC1809495/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809495/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17084275$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16178865$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aittoniemi, J.</creatorcontrib><creatorcontrib>Soranummi, H.</creatorcontrib><creatorcontrib>Rovio, A. T.</creatorcontrib><creatorcontrib>Hurme, M.</creatorcontrib><creatorcontrib>Pessi, T.</creatorcontrib><creatorcontrib>Nieminen, M.</creatorcontrib><creatorcontrib>Karjalainen, J.</creatorcontrib><title>Mannose‐binding lectin 2 (MBL2) gene polymorphism in asthma and atopy among adults</title><title>Clinical and experimental immunology</title><addtitle>Clin Exp Immunol</addtitle><description>Summary
Mannose‐binding lectin (MBL) insufficiency due to polymorphisms in the MBL2 gene causes an opsonization defect, which has been connected to infections and atopy. We investigated the significance of MBL2 genotypes with regard to persistent asthma and atopy among adults. The genotypes were determined in 243 adults with persistent asthma and 400 controls. Atopy was determined by skin‐prick test. As a result, the carriage of −221 base pairs (bp) promoter region variant allele X (nucleotide change G→C; alleles Y→X, respectively) causing low MBL expression proved to be a significant risk factor for asthma in non‐atopic males [odds ratio (OR) = 2·52, 95% confidence interval (CI) = 1·23–5·15; P = 0·01]. Furthermore, the X‐allele carriage was associated with the decrease in lung function (forced expiratory volume at 1 s, FEV1) during follow‐up in the patients with asthma (P = 0·033), the effect being strongest for non‐atopic asthmatics (P = 0·042). The MBL2 genotype had no clear effect on the occurrence of atopy in adults. In conclusion, our results abrogate the previously suggested predisposing effect of MBL insufficiency on atopy at least in adults. However, as MBL is a complement component participating in immune defence against microbes, and as in the pathogenesis of non‐atopic asthma infectious agents are probably involved, the gene–environment interactions between MBL and infections should be assessed further with regard to asthma.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>asthma</subject><subject>Asthma - immunology</subject><subject>Asthma - physiopathology</subject><subject>atopy</subject><subject>Biological and medical sciences</subject><subject>Female</subject><subject>Forced Expiratory Volume - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Genotype</subject><subject>Humans</subject><subject>Immunopathology</subject><subject>Male</subject><subject>Mannose-Binding Lectin - genetics</subject><subject>mannose‐binding lectin</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Original</subject><subject>Polymorphism, Genetic - genetics</subject><subject>Promoter Regions, Genetic - genetics</subject><issn>0009-9104</issn><issn>1365-2249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkcFu1DAURS0EokPhF5CFBCqLBNvjOPYCJDoqUGkqNmVtvTjOjEeOHeIEOjs-gW_kS0g6oxZY4Y1t3XOv3tNFCFOS0-m82eV0KYqMMa5yRkiREyYlzW8eoMWd8BAtCCEqU5TwE_Qkpd30FUKwx-iEClpKKYoFur6CEGKyv378rFyoXdhgb83gAmb47Op8zV7jjQ0Wd9Hv29h3W5daPKmQhm0LGEKNYYjdHkMbJy_Uox_SU_SoAZ_ss-N9ir58uLhefcrWnz9ert6vM1MwRTMramZsSRhYTlVFqrKhQkDJleAFNEBsXYqCCysba5rKkIobDlRIo9hS1Xx5it4dcruxam1tbBh68LrrXQv9Xkdw-m8luK3exG-aSqK4KqaAV8eAPn4dbRp065Kx3kOwcUxaSEELcgu--AfcxbEP03KaKiElYZROkDxApo8p9ba5m4QSPfemd3quR8_16Lk3fdubvpmsz__c5N54LGoCXh4BSAZ800MwLt1zJZGclTP39sB9d97u_3sAvbq4nF_L35awtJg</recordid><startdate>200510</startdate><enddate>200510</enddate><creator>Aittoniemi, J.</creator><creator>Soranummi, H.</creator><creator>Rovio, A. T.</creator><creator>Hurme, M.</creator><creator>Pessi, T.</creator><creator>Nieminen, M.</creator><creator>Karjalainen, J.</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><general>Oxford University Press</general><general>Blackwell Science Inc</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>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>M7N</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200510</creationdate><title>Mannose‐binding lectin 2 (MBL2) gene polymorphism in asthma and atopy among adults</title><author>Aittoniemi, J. ; Soranummi, H. ; Rovio, A. T. ; Hurme, M. ; Pessi, T. ; Nieminen, M. ; Karjalainen, J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5291-e6d2ce702ae419b0b7f166a749645afa0ed76546e8fecfbc0b4c4a168c9239d43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>asthma</topic><topic>Asthma - immunology</topic><topic>Asthma - physiopathology</topic><topic>atopy</topic><topic>Biological and medical sciences</topic><topic>Female</topic><topic>Forced Expiratory Volume - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Genotype</topic><topic>Humans</topic><topic>Immunopathology</topic><topic>Male</topic><topic>Mannose-Binding Lectin - genetics</topic><topic>mannose‐binding lectin</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Original</topic><topic>Polymorphism, Genetic - genetics</topic><topic>Promoter Regions, Genetic - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aittoniemi, J.</creatorcontrib><creatorcontrib>Soranummi, H.</creatorcontrib><creatorcontrib>Rovio, A. T.</creatorcontrib><creatorcontrib>Hurme, M.</creatorcontrib><creatorcontrib>Pessi, T.</creatorcontrib><creatorcontrib>Nieminen, M.</creatorcontrib><creatorcontrib>Karjalainen, J.</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>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>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>Aittoniemi, J.</au><au>Soranummi, H.</au><au>Rovio, A. T.</au><au>Hurme, M.</au><au>Pessi, T.</au><au>Nieminen, M.</au><au>Karjalainen, J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mannose‐binding lectin 2 (MBL2) gene polymorphism in asthma and atopy among adults</atitle><jtitle>Clinical and experimental immunology</jtitle><addtitle>Clin Exp Immunol</addtitle><date>2005-10</date><risdate>2005</risdate><volume>142</volume><issue>1</issue><spage>120</spage><epage>124</epage><pages>120-124</pages><issn>0009-9104</issn><eissn>1365-2249</eissn><coden>CEXIAL</coden><abstract>Summary
Mannose‐binding lectin (MBL) insufficiency due to polymorphisms in the MBL2 gene causes an opsonization defect, which has been connected to infections and atopy. We investigated the significance of MBL2 genotypes with regard to persistent asthma and atopy among adults. The genotypes were determined in 243 adults with persistent asthma and 400 controls. Atopy was determined by skin‐prick test. As a result, the carriage of −221 base pairs (bp) promoter region variant allele X (nucleotide change G→C; alleles Y→X, respectively) causing low MBL expression proved to be a significant risk factor for asthma in non‐atopic males [odds ratio (OR) = 2·52, 95% confidence interval (CI) = 1·23–5·15; P = 0·01]. Furthermore, the X‐allele carriage was associated with the decrease in lung function (forced expiratory volume at 1 s, FEV1) during follow‐up in the patients with asthma (P = 0·033), the effect being strongest for non‐atopic asthmatics (P = 0·042). The MBL2 genotype had no clear effect on the occurrence of atopy in adults. In conclusion, our results abrogate the previously suggested predisposing effect of MBL insufficiency on atopy at least in adults. However, as MBL is a complement component participating in immune defence against microbes, and as in the pathogenesis of non‐atopic asthma infectious agents are probably involved, the gene–environment interactions between MBL and infections should be assessed further with regard to asthma.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>16178865</pmid><doi>10.1111/j.1365-2249.2005.02881.x</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult Aged Aged, 80 and over asthma Asthma - immunology Asthma - physiopathology atopy Biological and medical sciences Female Forced Expiratory Volume - physiology Fundamental and applied biological sciences. Psychology Fundamental immunology Genetic Predisposition to Disease - genetics Genotype Humans Immunopathology Male Mannose-Binding Lectin - genetics mannose‐binding lectin Medical sciences Middle Aged Original Polymorphism, Genetic - genetics Promoter Regions, Genetic - genetics |
title | Mannose‐binding lectin 2 (MBL2) gene polymorphism in asthma and atopy among adults |
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