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Association of IL-10 polymorphism with severity of illness in community acquired pneumonia
Background: The influence of genetic polymorphisms of interleukin (IL)-10, tumour necrosis factor (TNF)-α, and IL-6 gene promoters on severity of systemic inflammatory response syndrome (SIRS) associated with community acquired pneumonia (CAP) was studied. Methods: Using PCR-RFLP analysis we analyse...
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Published in: | Thorax 2003-02, Vol.58 (2), p.154-156 |
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description | Background: The influence of genetic polymorphisms of interleukin (IL)-10, tumour necrosis factor (TNF)-α, and IL-6 gene promoters on severity of systemic inflammatory response syndrome (SIRS) associated with community acquired pneumonia (CAP) was studied. Methods: Using PCR-RFLP analysis we analysed a −1082G/A single nucleotide polymorphism (SNP) of the anti-inflammatory IL-10 gene, a −308G/A SNP of the pro-inflammatory TNF-α gene and a −174G/C SNP of the IL-6 gene. Illness severity was stratified according to SIRS score, calculated by presence of up to four physiological indices: temperature, white blood cell count, heart rate and respiratory rate (non-SIRS, SIRS 2, SIRS 3, and SIRS 4). Results: A statistically significant stepwise increase in frequency of the IL-10 G allele, associated with higher expression of the gene, was observed in patients with increasing severity of illness from non-SIRS (n=19) to SIRS 2 (n=17), SIRS 3 (n=33) and SIRS 4 (n=24). This was primarily due to a higher frequency of the GG genotype with increasing severity from non-SIRS through to SIRS 4. IL-10 G allele frequency was also increased in patients who died as a result of CAP (n=11) compared with CAP survivors (n=82) (p=0.01). No association was seen between the TNF-α −308G/A and IL-6 −174G/C SNPs and disease. Additionally, no interaction between all three SNP genotypes and disease severity was observed. Conclusions: A polymorphism affecting IL-10 expression may influence the severity of illness in patients with CAP. |
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Methods: Using PCR-RFLP analysis we analysed a −1082G/A single nucleotide polymorphism (SNP) of the anti-inflammatory IL-10 gene, a −308G/A SNP of the pro-inflammatory TNF-α gene and a −174G/C SNP of the IL-6 gene. Illness severity was stratified according to SIRS score, calculated by presence of up to four physiological indices: temperature, white blood cell count, heart rate and respiratory rate (non-SIRS, SIRS 2, SIRS 3, and SIRS 4). Results: A statistically significant stepwise increase in frequency of the IL-10 G allele, associated with higher expression of the gene, was observed in patients with increasing severity of illness from non-SIRS (n=19) to SIRS 2 (n=17), SIRS 3 (n=33) and SIRS 4 (n=24). This was primarily due to a higher frequency of the GG genotype with increasing severity from non-SIRS through to SIRS 4. IL-10 G allele frequency was also increased in patients who died as a result of CAP (n=11) compared with CAP survivors (n=82) (p=0.01). No association was seen between the TNF-α −308G/A and IL-6 −174G/C SNPs and disease. Additionally, no interaction between all three SNP genotypes and disease severity was observed. Conclusions: A polymorphism affecting IL-10 expression may influence the severity of illness in patients with CAP.</description><identifier>ISSN: 0040-6376</identifier><identifier>EISSN: 1468-3296</identifier><identifier>DOI: 10.1136/thorax.58.2.154</identifier><identifier>PMID: 12554901</identifier><identifier>CODEN: THORA7</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Thoracic Society</publisher><subject>Aged ; Aged, 80 and over ; Bacterial diseases ; Bacterial diseases of the respiratory system ; Bacterial pneumonia ; Biological and medical sciences ; Blood ; Case-Control Studies ; Chromosomes ; Chronic obstructive pulmonary disease ; community acquired pneumonia ; Community-Acquired Infections - genetics ; Cytokines ; Effectiveness ; Genetic aspects ; Human bacterial diseases ; Humans ; IL-10 polymorphism ; Illnesses ; Infectious diseases ; Interleukin-10 ; Interleukin-10 - genetics ; Interleukin-6 - genetics ; Medical sciences ; Physiological aspects ; Pneumonia ; Pneumonia - genetics ; Polymerase Chain Reaction - methods ; Polymorphism ; Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length ; Pulmonary Disease, Chronic Obstructive - complications ; Regression analysis ; Sepsis ; Short Paper ; Smoking - adverse effects ; systemic inflammatory response syndrome ; Systemic Inflammatory Response Syndrome - etiology ; Tumor Necrosis Factor-alpha - genetics ; Tumor necrosis factor-TNF</subject><ispartof>Thorax, 2003-02, Vol.58 (2), p.154-156</ispartof><rights>Copyright 2003 Thorax</rights><rights>2003 INIST-CNRS</rights><rights>COPYRIGHT 2003 BMJ Publishing Group Ltd.</rights><rights>Copyright: 2003 Copyright 2003 Thorax</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b595t-34e55e52dc4367b78fbf5eca28a0af21686f8b946130a653f4ed6b692bf0bb613</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1746580/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1746580/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14508190$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12554901$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gallagher, P M</creatorcontrib><creatorcontrib>Lowe, G</creatorcontrib><creatorcontrib>Fitzgerald, T</creatorcontrib><creatorcontrib>Bella, A</creatorcontrib><creatorcontrib>Greene, C M</creatorcontrib><creatorcontrib>McElvaney, N G</creatorcontrib><creatorcontrib>O’Neill, S J</creatorcontrib><title>Association of IL-10 polymorphism with severity of illness in community acquired pneumonia</title><title>Thorax</title><addtitle>Thorax</addtitle><description>Background: The influence of genetic polymorphisms of interleukin (IL)-10, tumour necrosis factor (TNF)-α, and IL-6 gene promoters on severity of systemic inflammatory response syndrome (SIRS) associated with community acquired pneumonia (CAP) was studied. Methods: Using PCR-RFLP analysis we analysed a −1082G/A single nucleotide polymorphism (SNP) of the anti-inflammatory IL-10 gene, a −308G/A SNP of the pro-inflammatory TNF-α gene and a −174G/C SNP of the IL-6 gene. Illness severity was stratified according to SIRS score, calculated by presence of up to four physiological indices: temperature, white blood cell count, heart rate and respiratory rate (non-SIRS, SIRS 2, SIRS 3, and SIRS 4). Results: A statistically significant stepwise increase in frequency of the IL-10 G allele, associated with higher expression of the gene, was observed in patients with increasing severity of illness from non-SIRS (n=19) to SIRS 2 (n=17), SIRS 3 (n=33) and SIRS 4 (n=24). This was primarily due to a higher frequency of the GG genotype with increasing severity from non-SIRS through to SIRS 4. IL-10 G allele frequency was also increased in patients who died as a result of CAP (n=11) compared with CAP survivors (n=82) (p=0.01). No association was seen between the TNF-α −308G/A and IL-6 −174G/C SNPs and disease. Additionally, no interaction between all three SNP genotypes and disease severity was observed. Conclusions: A polymorphism affecting IL-10 expression may influence the severity of illness in patients with CAP.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Bacterial diseases</subject><subject>Bacterial diseases of the respiratory system</subject><subject>Bacterial pneumonia</subject><subject>Biological and medical sciences</subject><subject>Blood</subject><subject>Case-Control Studies</subject><subject>Chromosomes</subject><subject>Chronic obstructive pulmonary disease</subject><subject>community acquired pneumonia</subject><subject>Community-Acquired Infections - genetics</subject><subject>Cytokines</subject><subject>Effectiveness</subject><subject>Genetic aspects</subject><subject>Human bacterial diseases</subject><subject>Humans</subject><subject>IL-10 polymorphism</subject><subject>Illnesses</subject><subject>Infectious diseases</subject><subject>Interleukin-10</subject><subject>Interleukin-10 - genetics</subject><subject>Interleukin-6 - genetics</subject><subject>Medical sciences</subject><subject>Physiological aspects</subject><subject>Pneumonia</subject><subject>Pneumonia - genetics</subject><subject>Polymerase Chain Reaction - methods</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Polymorphism, Restriction Fragment Length</subject><subject>Pulmonary Disease, Chronic Obstructive - complications</subject><subject>Regression analysis</subject><subject>Sepsis</subject><subject>Short Paper</subject><subject>Smoking - adverse effects</subject><subject>systemic inflammatory response syndrome</subject><subject>Systemic Inflammatory Response Syndrome - etiology</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor necrosis factor-TNF</subject><issn>0040-6376</issn><issn>1468-3296</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><recordid>eNqFkt2LEzEUxQdR3O7qs28yIPogTjeZTD7mRahl1dWiIKsLvoRMetOmO5N0k5l1-9-b0rJVWZA8BM795dx7w8myZxiNMSbstF_6oG7HVIzLMabVg2yEKyYKUtbsYTZCqEIFI5wdZccxrhBCAmP-ODvCJaVVjfAo-zmJ0Wureutd7k1-Piswyte-3XQ-rJc2dvkv2y_zCDcQbL_ZMrZtHcSYW5dr33WD2-pKXw82wDxfOxg676x6kj0yqo3wdH-fZN_fn11MPxazrx_Op5NZ0dCa9gWpgFKg5VxXhPGGC9MYClqVQiFlSswEM6KpK4YJUowSU8GcNawuG4OaJqkn2dud73poOphrcH1QrVwH26mwkV5Z-XfF2aVc-BuJecWoQMng1d4g-OsBYi87GzW0rXLghyh5WdekxiSBL_4BV34ILi2XvAQWiHHGEvVmRy1UC9I641NXvQAHqbl3YGySJ7VAXBDBE17cg6czh87q-_jTHa-DjzGAudsUI7kNhdyFQlIhS5lCkV48__ODDvw-BQl4uQdU1Ko1QTlt44GraApOjQ6j2tjD7V1dhSvJOOFUfvkxlZflxSf27ttneZn41zu-6Vb_nfI31T_fPQ</recordid><startdate>20030201</startdate><enddate>20030201</enddate><creator>Gallagher, P M</creator><creator>Lowe, G</creator><creator>Fitzgerald, T</creator><creator>Bella, A</creator><creator>Greene, C M</creator><creator>McElvaney, N G</creator><creator>O’Neill, S J</creator><general>BMJ Publishing Group Ltd and British Thoracic Society</general><general>BMJ</general><general>BMJ Publishing Group Ltd</general><general>BMJ Publishing Group LTD</general><general>BMJ Group</general><scope>BSCLL</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20030201</creationdate><title>Association of IL-10 polymorphism with severity of illness in community acquired pneumonia</title><author>Gallagher, P M ; Lowe, G ; Fitzgerald, T ; Bella, A ; Greene, C M ; McElvaney, N G ; O’Neill, S J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b595t-34e55e52dc4367b78fbf5eca28a0af21686f8b946130a653f4ed6b692bf0bb613</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Bacterial diseases</topic><topic>Bacterial diseases of the respiratory system</topic><topic>Bacterial pneumonia</topic><topic>Biological and medical sciences</topic><topic>Blood</topic><topic>Case-Control Studies</topic><topic>Chromosomes</topic><topic>Chronic obstructive pulmonary disease</topic><topic>community acquired pneumonia</topic><topic>Community-Acquired Infections - genetics</topic><topic>Cytokines</topic><topic>Effectiveness</topic><topic>Genetic aspects</topic><topic>Human bacterial diseases</topic><topic>Humans</topic><topic>IL-10 polymorphism</topic><topic>Illnesses</topic><topic>Infectious diseases</topic><topic>Interleukin-10</topic><topic>Interleukin-10 - genetics</topic><topic>Interleukin-6 - genetics</topic><topic>Medical sciences</topic><topic>Physiological aspects</topic><topic>Pneumonia</topic><topic>Pneumonia - genetics</topic><topic>Polymerase Chain Reaction - methods</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Polymorphism, Restriction Fragment Length</topic><topic>Pulmonary Disease, Chronic Obstructive - complications</topic><topic>Regression analysis</topic><topic>Sepsis</topic><topic>Short Paper</topic><topic>Smoking - adverse effects</topic><topic>systemic inflammatory response syndrome</topic><topic>Systemic Inflammatory Response Syndrome - etiology</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gallagher, P M</creatorcontrib><creatorcontrib>Lowe, G</creatorcontrib><creatorcontrib>Fitzgerald, T</creatorcontrib><creatorcontrib>Bella, A</creatorcontrib><creatorcontrib>Greene, C M</creatorcontrib><creatorcontrib>McElvaney, N G</creatorcontrib><creatorcontrib>O’Neill, S J</creatorcontrib><collection>Istex</collection><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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Thorax</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gallagher, P M</au><au>Lowe, G</au><au>Fitzgerald, T</au><au>Bella, A</au><au>Greene, C M</au><au>McElvaney, N G</au><au>O’Neill, S J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association of IL-10 polymorphism with severity of illness in community acquired pneumonia</atitle><jtitle>Thorax</jtitle><addtitle>Thorax</addtitle><date>2003-02-01</date><risdate>2003</risdate><volume>58</volume><issue>2</issue><spage>154</spage><epage>156</epage><pages>154-156</pages><issn>0040-6376</issn><eissn>1468-3296</eissn><coden>THORA7</coden><abstract>Background: The influence of genetic polymorphisms of interleukin (IL)-10, tumour necrosis factor (TNF)-α, and IL-6 gene promoters on severity of systemic inflammatory response syndrome (SIRS) associated with community acquired pneumonia (CAP) was studied. Methods: Using PCR-RFLP analysis we analysed a −1082G/A single nucleotide polymorphism (SNP) of the anti-inflammatory IL-10 gene, a −308G/A SNP of the pro-inflammatory TNF-α gene and a −174G/C SNP of the IL-6 gene. Illness severity was stratified according to SIRS score, calculated by presence of up to four physiological indices: temperature, white blood cell count, heart rate and respiratory rate (non-SIRS, SIRS 2, SIRS 3, and SIRS 4). Results: A statistically significant stepwise increase in frequency of the IL-10 G allele, associated with higher expression of the gene, was observed in patients with increasing severity of illness from non-SIRS (n=19) to SIRS 2 (n=17), SIRS 3 (n=33) and SIRS 4 (n=24). This was primarily due to a higher frequency of the GG genotype with increasing severity from non-SIRS through to SIRS 4. IL-10 G allele frequency was also increased in patients who died as a result of CAP (n=11) compared with CAP survivors (n=82) (p=0.01). No association was seen between the TNF-α −308G/A and IL-6 −174G/C SNPs and disease. Additionally, no interaction between all three SNP genotypes and disease severity was observed. Conclusions: A polymorphism affecting IL-10 expression may influence the severity of illness in patients with CAP.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Thoracic Society</pub><pmid>12554901</pmid><doi>10.1136/thorax.58.2.154</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aged Aged, 80 and over Bacterial diseases Bacterial diseases of the respiratory system Bacterial pneumonia Biological and medical sciences Blood Case-Control Studies Chromosomes Chronic obstructive pulmonary disease community acquired pneumonia Community-Acquired Infections - genetics Cytokines Effectiveness Genetic aspects Human bacterial diseases Humans IL-10 polymorphism Illnesses Infectious diseases Interleukin-10 Interleukin-10 - genetics Interleukin-6 - genetics Medical sciences Physiological aspects Pneumonia Pneumonia - genetics Polymerase Chain Reaction - methods Polymorphism Polymorphism, Genetic Polymorphism, Restriction Fragment Length Pulmonary Disease, Chronic Obstructive - complications Regression analysis Sepsis Short Paper Smoking - adverse effects systemic inflammatory response syndrome Systemic Inflammatory Response Syndrome - etiology Tumor Necrosis Factor-alpha - genetics Tumor necrosis factor-TNF |
title | Association of IL-10 polymorphism with severity of illness in community acquired pneumonia |
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