Imbalance of the interleukin 1 system in colonic mucosa—association with intestinal inflammation and interleukin 1 receptor agonist genotype 2

Background—Interleukin 1 (IL-1) α and β are potent cytokines which play key roles in inflammation. They are controlled by IL-1 receptor antagonist (IL-1ra). Aims—To investigate the influence of mucosal inflammation and IL-1ra genotype on the IL-1ra:IL-1 balance. Patients and methods—IL-1α, IL-1β, an...

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Published in:Gut 1997-11, Vol.41 (5), p.651-657
Main Authors: Andus, T, Daig, R, Vogl, D, Aschenbrenner, E, Lock, G, Hollerbach, S, Köllinger, M, Schölmerich, J, Gross, V
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Language:English
Subjects:
Biological and medical sciences
Biopsy
Colon
Crohn’s disease
Cytokines
Gastroenterology. Liver. Pancreas. Abdomen
genotype
Genotype & phenotype
Immune system
Inflammation
Inflammatory
Inflammatory bowel disease
interleukin 1
interleukin 1 receptor antagonist
Medical sciences
mucosal inflammation
Other diseases. Semiology
Proteins
Rodents
Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
Studies
Ulcers
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container_issue 5
container_start_page 651
container_title Gut
container_volume 41
creator Andus, T
Daig, R
Vogl, D
Aschenbrenner, E
Lock, G
Hollerbach, S
Köllinger, M
Schölmerich, J
Gross, V
description Background—Interleukin 1 (IL-1) α and β are potent cytokines which play key roles in inflammation. They are controlled by IL-1 receptor antagonist (IL-1ra). Aims—To investigate the influence of mucosal inflammation and IL-1ra genotype on the IL-1ra:IL-1 balance. Patients and methods—IL-1α, IL-1β, and IL-1ra were measured by enzyme linked immunosorbent assay (ELISA) in biopsy specimens taken from inflamed and non-inflamed colon of 60 patients with Crohn’s disease (CD), 34 with ulcerative colitis (UC), 15 inflammatory controls, and 103 non-inflamed controls. IL-1ra genotype was determined by polymerase chain reaction and gel electrophoresis. Results—IL-1α and IL-1β were significantly increased in inflamed mucosa in inflammatory bowel disease (IBD) (CD: 53.5 (22.4) and 409.9 (118.7) pg/mg protein, respectively; UC: 18.9 (6.8) and 214.5 (78.2) pg/mg, respectively) and non-IBD patients (19.2 (7.4) and 281.4 (121.0) pg/mg, respectively; p
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They are controlled by IL-1 receptor antagonist (IL-1ra). Aims—To investigate the influence of mucosal inflammation and IL-1ra genotype on the IL-1ra:IL-1 balance. Patients and methods—IL-1α, IL-1β, and IL-1ra were measured by enzyme linked immunosorbent assay (ELISA) in biopsy specimens taken from inflamed and non-inflamed colon of 60 patients with Crohn’s disease (CD), 34 with ulcerative colitis (UC), 15 inflammatory controls, and 103 non-inflamed controls. IL-1ra genotype was determined by polymerase chain reaction and gel electrophoresis. Results—IL-1α and IL-1β were significantly increased in inflamed mucosa in inflammatory bowel disease (IBD) (CD: 53.5 (22.4) and 409.9 (118.7) pg/mg protein, respectively; UC: 18.9 (6.8) and 214.5 (78.2) pg/mg, respectively) and non-IBD patients (19.2 (7.4) and 281.4 (121.0) pg/mg, respectively; p<0.0001) compared with normal controls (2.8 (0.6) and 30.6 (5.6) pg/mg, respectively). In CD IL-1α and β were also significantly increased in non-inflamed mucosa (6.1 (1.3) pg/mg and 88.7 (17.4) pg/mg, respectively; p<0.0012). IL-1ra:(IL-1α+β) ratios were significantly decreased in inflamed mucosa of patients with CD (182 (45); p<0.0001), UC (425 (136); p=0.0018) and without IBD (221 (76); p<0.0001), and in non-inflamed mucosa in CD (369 (149); p<0.0001) compared with normal controls (1307 (245); p<0.0001). Patients with IL-1ra genotype 2 had slightly but significantly reduced mucosal IL-1ra concentrations (p=0.003). The greatest difference was seen in colonic biopsy specimens from patients with inflamed Crohn’s disease. Conclusion—Mucosal inflammation can modulate the balance of the IL-1:IL-1ra system in colonic mucosa.]]></description><identifier>ISSN: 0017-5749</identifier><identifier>EISSN: 1468-3288</identifier><identifier>EISSN: 1458-3288</identifier><identifier>DOI: 10.1136/gut.41.5.651</identifier><identifier>PMID: 9414973</identifier><identifier>CODEN: GUTTAK</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Society of Gastroenterology</publisher><subject>Biological and medical sciences ; Biopsy ; Colon ; Crohn’s disease ; Cytokines ; Gastroenterology. Liver. Pancreas. Abdomen ; genotype ; Genotype &amp; phenotype ; Immune system ; Inflammation ; Inflammatory ; Inflammatory bowel disease ; interleukin 1 ; interleukin 1 receptor antagonist ; Medical sciences ; mucosal inflammation ; Other diseases. Semiology ; Proteins ; Rodents ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Studies ; Ulcers</subject><ispartof>Gut, 1997-11, Vol.41 (5), p.651-657</ispartof><rights>British Society of Gastroenterology</rights><rights>1998 INIST-CNRS</rights><rights>Copyright: 1997 British Society of Gastroenterology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b453t-41e4dc355af96d9272a34224a5868b3091fd0f0df9c48c636d97ff045dac8cd43</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/PMC1891562/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1891562/$$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&amp;idt=2045620$$DView record in Pascal Francis$$Hfree_for_read</backlink></links><search><creatorcontrib>Andus, T</creatorcontrib><creatorcontrib>Daig, R</creatorcontrib><creatorcontrib>Vogl, D</creatorcontrib><creatorcontrib>Aschenbrenner, E</creatorcontrib><creatorcontrib>Lock, G</creatorcontrib><creatorcontrib>Hollerbach, S</creatorcontrib><creatorcontrib>Köllinger, M</creatorcontrib><creatorcontrib>Schölmerich, J</creatorcontrib><creatorcontrib>Gross, V</creatorcontrib><title>Imbalance of the interleukin 1 system in colonic mucosa—association with intestinal inflammation and interleukin 1 receptor agonist genotype 2</title><title>Gut</title><addtitle>Gut</addtitle><description><![CDATA[Background—Interleukin 1 (IL-1) α and β are potent cytokines which play key roles in inflammation. They are controlled by IL-1 receptor antagonist (IL-1ra). Aims—To investigate the influence of mucosal inflammation and IL-1ra genotype on the IL-1ra:IL-1 balance. Patients and methods—IL-1α, IL-1β, and IL-1ra were measured by enzyme linked immunosorbent assay (ELISA) in biopsy specimens taken from inflamed and non-inflamed colon of 60 patients with Crohn’s disease (CD), 34 with ulcerative colitis (UC), 15 inflammatory controls, and 103 non-inflamed controls. IL-1ra genotype was determined by polymerase chain reaction and gel electrophoresis. Results—IL-1α and IL-1β were significantly increased in inflamed mucosa in inflammatory bowel disease (IBD) (CD: 53.5 (22.4) and 409.9 (118.7) pg/mg protein, respectively; UC: 18.9 (6.8) and 214.5 (78.2) pg/mg, respectively) and non-IBD patients (19.2 (7.4) and 281.4 (121.0) pg/mg, respectively; p<0.0001) compared with normal controls (2.8 (0.6) and 30.6 (5.6) pg/mg, respectively). In CD IL-1α and β were also significantly increased in non-inflamed mucosa (6.1 (1.3) pg/mg and 88.7 (17.4) pg/mg, respectively; p<0.0012). IL-1ra:(IL-1α+β) ratios were significantly decreased in inflamed mucosa of patients with CD (182 (45); p<0.0001), UC (425 (136); p=0.0018) and without IBD (221 (76); p<0.0001), and in non-inflamed mucosa in CD (369 (149); p<0.0001) compared with normal controls (1307 (245); p<0.0001). Patients with IL-1ra genotype 2 had slightly but significantly reduced mucosal IL-1ra concentrations (p=0.003). The greatest difference was seen in colonic biopsy specimens from patients with inflamed Crohn’s disease. Conclusion—Mucosal inflammation can modulate the balance of the IL-1:IL-1ra system in colonic mucosa.]]></description><subject>Biological and medical sciences</subject><subject>Biopsy</subject><subject>Colon</subject><subject>Crohn’s disease</subject><subject>Cytokines</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>genotype</subject><subject>Genotype &amp; phenotype</subject><subject>Immune system</subject><subject>Inflammation</subject><subject>Inflammatory</subject><subject>Inflammatory bowel disease</subject><subject>interleukin 1</subject><subject>interleukin 1 receptor antagonist</subject><subject>Medical sciences</subject><subject>mucosal inflammation</subject><subject>Other diseases. Semiology</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. 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Liver. Pancreas. Abdomen</topic><topic>genotype</topic><topic>Genotype &amp; phenotype</topic><topic>Immune system</topic><topic>Inflammation</topic><topic>Inflammatory</topic><topic>Inflammatory bowel disease</topic><topic>interleukin 1</topic><topic>interleukin 1 receptor antagonist</topic><topic>Medical sciences</topic><topic>mucosal inflammation</topic><topic>Other diseases. Semiology</topic><topic>Proteins</topic><topic>Rodents</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Studies</topic><topic>Ulcers</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Andus, T</creatorcontrib><creatorcontrib>Daig, R</creatorcontrib><creatorcontrib>Vogl, D</creatorcontrib><creatorcontrib>Aschenbrenner, E</creatorcontrib><creatorcontrib>Lock, G</creatorcontrib><creatorcontrib>Hollerbach, S</creatorcontrib><creatorcontrib>Köllinger, M</creatorcontrib><creatorcontrib>Schölmerich, J</creatorcontrib><creatorcontrib>Gross, V</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>ProQuest Biological Science Journals</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>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Gut</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Andus, T</au><au>Daig, R</au><au>Vogl, D</au><au>Aschenbrenner, E</au><au>Lock, G</au><au>Hollerbach, S</au><au>Köllinger, M</au><au>Schölmerich, J</au><au>Gross, V</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Imbalance of the interleukin 1 system in colonic mucosa—association with intestinal inflammation and interleukin 1 receptor agonist genotype 2</atitle><jtitle>Gut</jtitle><addtitle>Gut</addtitle><date>1997-11-01</date><risdate>1997</risdate><volume>41</volume><issue>5</issue><spage>651</spage><epage>657</epage><pages>651-657</pages><issn>0017-5749</issn><eissn>1468-3288</eissn><eissn>1458-3288</eissn><coden>GUTTAK</coden><abstract><![CDATA[Background—Interleukin 1 (IL-1) α and β are potent cytokines which play key roles in inflammation. They are controlled by IL-1 receptor antagonist (IL-1ra). Aims—To investigate the influence of mucosal inflammation and IL-1ra genotype on the IL-1ra:IL-1 balance. Patients and methods—IL-1α, IL-1β, and IL-1ra were measured by enzyme linked immunosorbent assay (ELISA) in biopsy specimens taken from inflamed and non-inflamed colon of 60 patients with Crohn’s disease (CD), 34 with ulcerative colitis (UC), 15 inflammatory controls, and 103 non-inflamed controls. IL-1ra genotype was determined by polymerase chain reaction and gel electrophoresis. Results—IL-1α and IL-1β were significantly increased in inflamed mucosa in inflammatory bowel disease (IBD) (CD: 53.5 (22.4) and 409.9 (118.7) pg/mg protein, respectively; UC: 18.9 (6.8) and 214.5 (78.2) pg/mg, respectively) and non-IBD patients (19.2 (7.4) and 281.4 (121.0) pg/mg, respectively; p<0.0001) compared with normal controls (2.8 (0.6) and 30.6 (5.6) pg/mg, respectively). In CD IL-1α and β were also significantly increased in non-inflamed mucosa (6.1 (1.3) pg/mg and 88.7 (17.4) pg/mg, respectively; p<0.0012). IL-1ra:(IL-1α+β) ratios were significantly decreased in inflamed mucosa of patients with CD (182 (45); p<0.0001), UC (425 (136); p=0.0018) and without IBD (221 (76); p<0.0001), and in non-inflamed mucosa in CD (369 (149); p<0.0001) compared with normal controls (1307 (245); p<0.0001). Patients with IL-1ra genotype 2 had slightly but significantly reduced mucosal IL-1ra concentrations (p=0.003). The greatest difference was seen in colonic biopsy specimens from patients with inflamed Crohn’s disease. Conclusion—Mucosal inflammation can modulate the balance of the IL-1:IL-1ra system in colonic mucosa.]]></abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Society of Gastroenterology</pub><pmid>9414973</pmid><doi>10.1136/gut.41.5.651</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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source Open Access: PubMed Central
subjects Biological and medical sciences
Biopsy
Colon
Crohn’s disease
Cytokines
Gastroenterology. Liver. Pancreas. Abdomen
genotype
Genotype & phenotype
Immune system
Inflammation
Inflammatory
Inflammatory bowel disease
interleukin 1
interleukin 1 receptor antagonist
Medical sciences
mucosal inflammation
Other diseases. Semiology
Proteins
Rodents
Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
Studies
Ulcers
title Imbalance of the interleukin 1 system in colonic mucosa—association with intestinal inflammation and interleukin 1 receptor agonist genotype 2
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