Effect of interleukin 1 polymorphisms on gastric mucosal interleukin 1beta production in Helicobacter pylori infection
Although epidemiological studies suggest that interleukin (IL)-1 genetic polymorphisms are involved in Helicobacter pylori-related gastric carcinogenesis, the data are conflicting regarding the effects of these polymorphisms on IL-1beta production. IL-1B-511 polymorphism was genotyped by polymerase...
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| Veröffentlicht in: | Gastroenterology (New York, N.Y. 1943) N.Y. 1943), 2002-12, Vol.123 (6), p.1793 |
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| creator | Hwang, Il-Ran Kodama, Tadashi Kikuchi, Shogo Sakai, Kyoko Peterson, Leif E Graham, David Y Yamaoka, Yoshio |
| description | Although epidemiological studies suggest that interleukin (IL)-1 genetic polymorphisms are involved in Helicobacter pylori-related gastric carcinogenesis, the data are conflicting regarding the effects of these polymorphisms on IL-1beta production.
IL-1B-511 polymorphism was genotyped by polymerase chain reaction (PCR)-restriction fragment length polymorphism, and IL-1RN variable number of tandem repeats was determined by PCR. Mucosal IL-1beta levels were measured by enzyme-linked immunosorbent assay. To determine which factors influence mucosal IL-1beta levels, gastric inflammation, and atrophy, multiple regression analyses were performed.
We studied 117 H. pylori-infected Japanese patients. Carriers of the IL-1B-511T/T genotype or IL-1RN*2 allele had higher mucosal IL-1beta levels than noncarriers (partial regression coefficient [PRC] +/- SE), TT versus CC: 37.6 +/- 6 [antrum] and 32.1 +/- 6 [corpus] pg/mg protein (P < 0.001 for each), *1/*2 versus *1/*1: 24 +/- 8 [antrum] (P |
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IL-1B-511 polymorphism was genotyped by polymerase chain reaction (PCR)-restriction fragment length polymorphism, and IL-1RN variable number of tandem repeats was determined by PCR. Mucosal IL-1beta levels were measured by enzyme-linked immunosorbent assay. To determine which factors influence mucosal IL-1beta levels, gastric inflammation, and atrophy, multiple regression analyses were performed.
We studied 117 H. pylori-infected Japanese patients. Carriers of the IL-1B-511T/T genotype or IL-1RN*2 allele had higher mucosal IL-1beta levels than noncarriers (partial regression coefficient [PRC] +/- SE), TT versus CC: 37.6 +/- 6 [antrum] and 32.1 +/- 6 [corpus] pg/mg protein (P < 0.001 for each), *1/*2 versus *1/*1: 24 +/- 8 [antrum] (P <0.01) and 36.5 +/- 7 [corpus] (P <0.001). Simultaneous carriers of IL-1B-511T/T genotype and IL-1RN*2 allele had the highest IL-1beta levels (82.9 +/- 12 [antrum] and 87.2 +/- 11 [corpus]) and showed a synergistic effect between 2 loci. The *1/*2 carriers were closely related to atrophy (PRC +/- SE; 0.87 +/- 0.4 [antrum] and 0.93 +/- 0.4 [corpus], P < 0.05), whereas being a carrier of the -511T/T genotype was related to severe gastric inflammation.
IL-1 genetic polymorphisms influenced H. pylori-related gastric mucosal IL-1beta levels and were related to gastric inflammation and atrophy, factors thought to be important in gastric carcinogenesis.</description><identifier>ISSN: 0016-5085</identifier><identifier>PMID: 12454835</identifier><language>eng</language><publisher>United States</publisher><subject>Adult ; Aged ; Atrophy ; Colony Count, Microbial ; Female ; Gastric Mucosa - metabolism ; Helicobacter Infections - genetics ; Helicobacter Infections - metabolism ; Helicobacter Infections - microbiology ; Helicobacter Infections - pathology ; Helicobacter pylori ; Humans ; Interleukin-1 - biosynthesis ; Interleukin-1 - genetics ; Male ; Middle Aged ; Monocytes - pathology ; Neutrophil Infiltration ; Polymorphism, Genetic ; Stomach - metabolism ; Stomach - pathology</subject><ispartof>Gastroenterology (New York, N.Y. 1943), 2002-12, Vol.123 (6), p.1793</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12454835$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hwang, Il-Ran</creatorcontrib><creatorcontrib>Kodama, Tadashi</creatorcontrib><creatorcontrib>Kikuchi, Shogo</creatorcontrib><creatorcontrib>Sakai, Kyoko</creatorcontrib><creatorcontrib>Peterson, Leif E</creatorcontrib><creatorcontrib>Graham, David Y</creatorcontrib><creatorcontrib>Yamaoka, Yoshio</creatorcontrib><title>Effect of interleukin 1 polymorphisms on gastric mucosal interleukin 1beta production in Helicobacter pylori infection</title><title>Gastroenterology (New York, N.Y. 1943)</title><addtitle>Gastroenterology</addtitle><description>Although epidemiological studies suggest that interleukin (IL)-1 genetic polymorphisms are involved in Helicobacter pylori-related gastric carcinogenesis, the data are conflicting regarding the effects of these polymorphisms on IL-1beta production.
IL-1B-511 polymorphism was genotyped by polymerase chain reaction (PCR)-restriction fragment length polymorphism, and IL-1RN variable number of tandem repeats was determined by PCR. Mucosal IL-1beta levels were measured by enzyme-linked immunosorbent assay. To determine which factors influence mucosal IL-1beta levels, gastric inflammation, and atrophy, multiple regression analyses were performed.
We studied 117 H. pylori-infected Japanese patients. Carriers of the IL-1B-511T/T genotype or IL-1RN*2 allele had higher mucosal IL-1beta levels than noncarriers (partial regression coefficient [PRC] +/- SE), TT versus CC: 37.6 +/- 6 [antrum] and 32.1 +/- 6 [corpus] pg/mg protein (P < 0.001 for each), *1/*2 versus *1/*1: 24 +/- 8 [antrum] (P <0.01) and 36.5 +/- 7 [corpus] (P <0.001). Simultaneous carriers of IL-1B-511T/T genotype and IL-1RN*2 allele had the highest IL-1beta levels (82.9 +/- 12 [antrum] and 87.2 +/- 11 [corpus]) and showed a synergistic effect between 2 loci. The *1/*2 carriers were closely related to atrophy (PRC +/- SE; 0.87 +/- 0.4 [antrum] and 0.93 +/- 0.4 [corpus], P < 0.05), whereas being a carrier of the -511T/T genotype was related to severe gastric inflammation.
IL-1 genetic polymorphisms influenced H. pylori-related gastric mucosal IL-1beta levels and were related to gastric inflammation and atrophy, factors thought to be important in gastric carcinogenesis.</description><subject>Adult</subject><subject>Aged</subject><subject>Atrophy</subject><subject>Colony Count, Microbial</subject><subject>Female</subject><subject>Gastric Mucosa - metabolism</subject><subject>Helicobacter Infections - genetics</subject><subject>Helicobacter Infections - metabolism</subject><subject>Helicobacter Infections - microbiology</subject><subject>Helicobacter Infections - pathology</subject><subject>Helicobacter pylori</subject><subject>Humans</subject><subject>Interleukin-1 - biosynthesis</subject><subject>Interleukin-1 - genetics</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Monocytes - pathology</subject><subject>Neutrophil Infiltration</subject><subject>Polymorphism, Genetic</subject><subject>Stomach - metabolism</subject><subject>Stomach - pathology</subject><issn>0016-5085</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVj8tKAzEARbNQbK3-guQHBpLJo5mllGqFQjfdlzw1mpmEJCPM3xtRF64uXA73cq7AGiHMO4YEW4HbUt4RQgMR-AascE8ZFYStwefeOasrjA76qdoc7PzhJ4hhimEZY05vvowFxgm-ylKz13CcdSwy_MeVrRKmHM2sq29w6w42eB2V1A2DaQkx-1Z_nzXgDlw7GYq9_80NOD_tz7tDdzw9v-wej11ilHVC4Z5pgpQghCozGCq3thec2iZGtR6wEk1PckYQZ4o4bZCjWGLmthxxQjbg4Wc2zWq05pKyH2VeLn_-5AvObVfu</recordid><startdate>200212</startdate><enddate>200212</enddate><creator>Hwang, Il-Ran</creator><creator>Kodama, Tadashi</creator><creator>Kikuchi, Shogo</creator><creator>Sakai, Kyoko</creator><creator>Peterson, Leif E</creator><creator>Graham, David Y</creator><creator>Yamaoka, Yoshio</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>200212</creationdate><title>Effect of interleukin 1 polymorphisms on gastric mucosal interleukin 1beta production in Helicobacter pylori infection</title><author>Hwang, Il-Ran ; Kodama, Tadashi ; Kikuchi, Shogo ; Sakai, Kyoko ; Peterson, Leif E ; Graham, David Y ; Yamaoka, Yoshio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p545-8b125c30b8334bd9d4a7e2864e0164cc91b8508a653065b3fcd0f41a15f760633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Atrophy</topic><topic>Colony Count, Microbial</topic><topic>Female</topic><topic>Gastric Mucosa - metabolism</topic><topic>Helicobacter Infections - genetics</topic><topic>Helicobacter Infections - metabolism</topic><topic>Helicobacter Infections - microbiology</topic><topic>Helicobacter Infections - pathology</topic><topic>Helicobacter pylori</topic><topic>Humans</topic><topic>Interleukin-1 - biosynthesis</topic><topic>Interleukin-1 - genetics</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Monocytes - pathology</topic><topic>Neutrophil Infiltration</topic><topic>Polymorphism, Genetic</topic><topic>Stomach - metabolism</topic><topic>Stomach - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hwang, Il-Ran</creatorcontrib><creatorcontrib>Kodama, Tadashi</creatorcontrib><creatorcontrib>Kikuchi, Shogo</creatorcontrib><creatorcontrib>Sakai, Kyoko</creatorcontrib><creatorcontrib>Peterson, Leif E</creatorcontrib><creatorcontrib>Graham, David Y</creatorcontrib><creatorcontrib>Yamaoka, Yoshio</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Gastroenterology (New York, N.Y. 1943)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hwang, Il-Ran</au><au>Kodama, Tadashi</au><au>Kikuchi, Shogo</au><au>Sakai, Kyoko</au><au>Peterson, Leif E</au><au>Graham, David Y</au><au>Yamaoka, Yoshio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of interleukin 1 polymorphisms on gastric mucosal interleukin 1beta production in Helicobacter pylori infection</atitle><jtitle>Gastroenterology (New York, N.Y. 1943)</jtitle><addtitle>Gastroenterology</addtitle><date>2002-12</date><risdate>2002</risdate><volume>123</volume><issue>6</issue><spage>1793</spage><pages>1793-</pages><issn>0016-5085</issn><abstract>Although epidemiological studies suggest that interleukin (IL)-1 genetic polymorphisms are involved in Helicobacter pylori-related gastric carcinogenesis, the data are conflicting regarding the effects of these polymorphisms on IL-1beta production.
IL-1B-511 polymorphism was genotyped by polymerase chain reaction (PCR)-restriction fragment length polymorphism, and IL-1RN variable number of tandem repeats was determined by PCR. Mucosal IL-1beta levels were measured by enzyme-linked immunosorbent assay. To determine which factors influence mucosal IL-1beta levels, gastric inflammation, and atrophy, multiple regression analyses were performed.
We studied 117 H. pylori-infected Japanese patients. Carriers of the IL-1B-511T/T genotype or IL-1RN*2 allele had higher mucosal IL-1beta levels than noncarriers (partial regression coefficient [PRC] +/- SE), TT versus CC: 37.6 +/- 6 [antrum] and 32.1 +/- 6 [corpus] pg/mg protein (P < 0.001 for each), *1/*2 versus *1/*1: 24 +/- 8 [antrum] (P <0.01) and 36.5 +/- 7 [corpus] (P <0.001). Simultaneous carriers of IL-1B-511T/T genotype and IL-1RN*2 allele had the highest IL-1beta levels (82.9 +/- 12 [antrum] and 87.2 +/- 11 [corpus]) and showed a synergistic effect between 2 loci. The *1/*2 carriers were closely related to atrophy (PRC +/- SE; 0.87 +/- 0.4 [antrum] and 0.93 +/- 0.4 [corpus], P < 0.05), whereas being a carrier of the -511T/T genotype was related to severe gastric inflammation.
IL-1 genetic polymorphisms influenced H. pylori-related gastric mucosal IL-1beta levels and were related to gastric inflammation and atrophy, factors thought to be important in gastric carcinogenesis.</abstract><cop>United States</cop><pmid>12454835</pmid></addata></record> |
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| ispartof | Gastroenterology (New York, N.Y. 1943), 2002-12, Vol.123 (6), p.1793 |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete; Alma/SFX Local Collection |
| subjects | Adult Aged Atrophy Colony Count, Microbial Female Gastric Mucosa - metabolism Helicobacter Infections - genetics Helicobacter Infections - metabolism Helicobacter Infections - microbiology Helicobacter Infections - pathology Helicobacter pylori Humans Interleukin-1 - biosynthesis Interleukin-1 - genetics Male Middle Aged Monocytes - pathology Neutrophil Infiltration Polymorphism, Genetic Stomach - metabolism Stomach - pathology |
| title | Effect of interleukin 1 polymorphisms on gastric mucosal interleukin 1beta production in Helicobacter pylori infection |
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