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Intercellular adhesion molecule‐1 (ICAM‐1) deficiency protects mice against severe forms of experimentally induced colitis
ICAM‐1 (CD54), the ligand for LFA‐1 and Mac‐1, is up‐regulated during inflammatory reaction on the activated vascular endothelium. To determine its role in intestinal inflammation, we induced acute experimental colitis in mice with a deleted ICAM‐1 gene, by feeding them with 3% dextran sodium sulpha...
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| Published in: | Clinical and experimental immunology 2000-01, Vol.119 (1), p.57-63 |
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| container_title | Clinical and experimental immunology |
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| creator | Bendjelloul, F. Malý, P. Mandys, V. Jirkovská, M. Prokešová, L. Tučková, L. Tlaskalová‐Hogenová, H. |
| description | ICAM‐1 (CD54), the ligand for LFA‐1 and Mac‐1, is up‐regulated during inflammatory reaction on the activated vascular endothelium. To determine its role in intestinal inflammation, we induced acute experimental colitis in mice with a deleted ICAM‐1 gene, by feeding them with 3% dextran sodium sulphate (DSS) in drinking water for 7 days. Chronic colitis was elicited by DSS similarly, followed by 2 weeks with water. In the acute phase of inflammation, ICAM‐1‐deficient mice exhibited a significantly lower mortality rate (5%) than control C57Bl/6J mice (35%). Control animals, but not the ICAM‐1‐deficient mice, exhibited diarrhoea and rectal bleeding. Histological examination of large‐bowel samples evaluated the intensity of inflammatory changes, and type and extent of mucosal lesions. In the acute phase, 33.3% of samples from ICAM‐1‐deficient mice exhibited mucosal defects (flat and fissural ulcers), predominantly mild to moderate inflammatory infiltrate within the lamina propria mucosae and lower grades of mucosal lesions. Much stronger inflammatory changes were present in control animals, flat ulcers (sometimes multiple) and fissural ulcers being observed in 62.5% of samples. Mucosal inflammatory infiltrate was moderate to severe, typically with higher grades of mucosal lesions. In chronic colitis, smaller inflammatory changes were found in the large bowel. The two mouse strains differed, the chronic colitis being accompanied by an increased serum level of anti‐epithelial IgA autoantibodies in C57Bl/6 control mice but not in ICAM‐1‐deficient mice. These findings provide direct evidence of the participation of ICAM‐1 molecule in the development of experimentally induced intestinal inflammation. |
| doi_str_mv | 10.1046/j.1365-2249.2000.01090.x |
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To determine its role in intestinal inflammation, we induced acute experimental colitis in mice with a deleted ICAM‐1 gene, by feeding them with 3% dextran sodium sulphate (DSS) in drinking water for 7 days. Chronic colitis was elicited by DSS similarly, followed by 2 weeks with water. In the acute phase of inflammation, ICAM‐1‐deficient mice exhibited a significantly lower mortality rate (5%) than control C57Bl/6J mice (35%). Control animals, but not the ICAM‐1‐deficient mice, exhibited diarrhoea and rectal bleeding. Histological examination of large‐bowel samples evaluated the intensity of inflammatory changes, and type and extent of mucosal lesions. In the acute phase, 33.3% of samples from ICAM‐1‐deficient mice exhibited mucosal defects (flat and fissural ulcers), predominantly mild to moderate inflammatory infiltrate within the lamina propria mucosae and lower grades of mucosal lesions. Much stronger inflammatory changes were present in control animals, flat ulcers (sometimes multiple) and fissural ulcers being observed in 62.5% of samples. Mucosal inflammatory infiltrate was moderate to severe, typically with higher grades of mucosal lesions. In chronic colitis, smaller inflammatory changes were found in the large bowel. The two mouse strains differed, the chronic colitis being accompanied by an increased serum level of anti‐epithelial IgA autoantibodies in C57Bl/6 control mice but not in ICAM‐1‐deficient mice. These findings provide direct evidence of the participation of ICAM‐1 molecule in the development of experimentally induced intestinal inflammation.</description><identifier>ISSN: 0009-9104</identifier><identifier>EISSN: 1365-2249</identifier><identifier>DOI: 10.1046/j.1365-2249.2000.01090.x</identifier><identifier>PMID: 10606964</identifier><identifier>CODEN: CEXIAL</identifier><language>eng</language><publisher>Oxford BSL: Blackwell Science Ltd</publisher><subject>Animals ; Autoantibodies - blood ; Biological and medical sciences ; Colitis - etiology ; Colitis - pathology ; Colitis - prevention & control ; Dextran Sulfate - administration & dosage ; Dextran Sulfate - toxicity ; Disease Models, Animal ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; gene knock‐out ; Gut Disease ; Immunoglobulin A - blood ; Intercellular Adhesion Molecule-1 - genetics ; Intercellular Adhesion Molecule-1 - physiology ; intercellular adhesion molecule‐1 ; intestinal inflammation ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Other diseases. Semiology ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; ulcerative colitis adhesion molecules</subject><ispartof>Clinical and experimental immunology, 2000-01, Vol.119 (1), p.57-63</ispartof><rights>2000 INIST-CNRS</rights><rights>Copyright Blackwell Scientific Publications Ltd. Jan 2000</rights><rights>2000 Blackwell Science Ltd 2000</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5920-4fa25d2f3919a67ce602b7b12bbd4900ec4e8798ecb6a0230ccbc44086ea16563</citedby><cites>FETCH-LOGICAL-c5920-4fa25d2f3919a67ce602b7b12bbd4900ec4e8798ecb6a0230ccbc44086ea16563</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1365-2249.2000.01090.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1365-2249.2000.01090.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,315,733,786,790,891,27957,27958,50923,51032,53827,53829</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1251340$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10606964$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bendjelloul, F.</creatorcontrib><creatorcontrib>Malý, P.</creatorcontrib><creatorcontrib>Mandys, V.</creatorcontrib><creatorcontrib>Jirkovská, M.</creatorcontrib><creatorcontrib>Prokešová, L.</creatorcontrib><creatorcontrib>Tučková, L.</creatorcontrib><creatorcontrib>Tlaskalová‐Hogenová, H.</creatorcontrib><title>Intercellular adhesion molecule‐1 (ICAM‐1) deficiency protects mice against severe forms of experimentally induced colitis</title><title>Clinical and experimental immunology</title><addtitle>Clin Exp Immunol</addtitle><description>ICAM‐1 (CD54), the ligand for LFA‐1 and Mac‐1, is up‐regulated during inflammatory reaction on the activated vascular endothelium. To determine its role in intestinal inflammation, we induced acute experimental colitis in mice with a deleted ICAM‐1 gene, by feeding them with 3% dextran sodium sulphate (DSS) in drinking water for 7 days. Chronic colitis was elicited by DSS similarly, followed by 2 weeks with water. In the acute phase of inflammation, ICAM‐1‐deficient mice exhibited a significantly lower mortality rate (5%) than control C57Bl/6J mice (35%). Control animals, but not the ICAM‐1‐deficient mice, exhibited diarrhoea and rectal bleeding. Histological examination of large‐bowel samples evaluated the intensity of inflammatory changes, and type and extent of mucosal lesions. In the acute phase, 33.3% of samples from ICAM‐1‐deficient mice exhibited mucosal defects (flat and fissural ulcers), predominantly mild to moderate inflammatory infiltrate within the lamina propria mucosae and lower grades of mucosal lesions. Much stronger inflammatory changes were present in control animals, flat ulcers (sometimes multiple) and fissural ulcers being observed in 62.5% of samples. Mucosal inflammatory infiltrate was moderate to severe, typically with higher grades of mucosal lesions. In chronic colitis, smaller inflammatory changes were found in the large bowel. The two mouse strains differed, the chronic colitis being accompanied by an increased serum level of anti‐epithelial IgA autoantibodies in C57Bl/6 control mice but not in ICAM‐1‐deficient mice. These findings provide direct evidence of the participation of ICAM‐1 molecule in the development of experimentally induced intestinal inflammation.</description><subject>Animals</subject><subject>Autoantibodies - blood</subject><subject>Biological and medical sciences</subject><subject>Colitis - etiology</subject><subject>Colitis - pathology</subject><subject>Colitis - prevention & control</subject><subject>Dextran Sulfate - administration & dosage</subject><subject>Dextran Sulfate - toxicity</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>gene knock‐out</subject><subject>Gut Disease</subject><subject>Immunoglobulin A - blood</subject><subject>Intercellular Adhesion Molecule-1 - genetics</subject><subject>Intercellular Adhesion Molecule-1 - physiology</subject><subject>intercellular adhesion molecule‐1</subject><subject>intestinal inflammation</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Other diseases. Semiology</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>ulcerative colitis adhesion molecules</subject><issn>0009-9104</issn><issn>1365-2249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><recordid>eNqNkcGO0zAURS0EYsrALyALsYBFwrPjuPUCJFQNUGkQG1hbjvMy48qJi50M7QbxCXwjX4JDq2HYsfKz3rn3XekSQhmUDIR8tS1ZJeuCc6FKDgAlMFBQ7u-Rxe3iPlnkjSpUVpyRRylt81dKyR-SMwYSpJJiQb5vhhGjRe8nbyI17TUmFwbaB4928vjrx09GX2zWbz_O00vaYuesw8Ee6C6GEe2YaO8sUnNl3JBGmvAGI9IuxD7R0FHc7zC6HofReH-gbmgniy21wbvRpcfkQWd8wien95x8eXfxef2huPz0Ph-9LGytOBSiM7xueVcppoxcWpTAm2XDeNO0QgGgFbhaqhXaRhrgFVjbWCFgJdEwWcvqnLw5-u6mpsfW5jjReL3LyUw86GCc_nczuGt9FW40U1DXgmeDZyeDGL5OmEa9DVMccuaMyJWEWogMrY6QjSGliN3tAQZ6Lk5v9dyPnvvRc3H6T3F6n6VP7wa8Izw2lYHnJ8Aka3wXzWBd-svxmlUCMvb6iH1zHg__fV-vLzbzVP0GRA636Q</recordid><startdate>200001</startdate><enddate>200001</enddate><creator>Bendjelloul, F.</creator><creator>Malý, P.</creator><creator>Mandys, V.</creator><creator>Jirkovská, M.</creator><creator>Prokešová, L.</creator><creator>Tučková, L.</creator><creator>Tlaskalová‐Hogenová, H.</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>5PM</scope></search><sort><creationdate>200001</creationdate><title>Intercellular adhesion molecule‐1 (ICAM‐1) deficiency protects mice against severe forms of experimentally induced colitis</title><author>Bendjelloul, F. ; Malý, P. ; Mandys, V. ; Jirkovská, M. ; Prokešová, L. ; Tučková, L. ; Tlaskalová‐Hogenová, H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5920-4fa25d2f3919a67ce602b7b12bbd4900ec4e8798ecb6a0230ccbc44086ea16563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Autoantibodies - blood</topic><topic>Biological and medical sciences</topic><topic>Colitis - etiology</topic><topic>Colitis - pathology</topic><topic>Colitis - prevention & control</topic><topic>Dextran Sulfate - administration & dosage</topic><topic>Dextran Sulfate - toxicity</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>gene knock‐out</topic><topic>Gut Disease</topic><topic>Immunoglobulin A - blood</topic><topic>Intercellular Adhesion Molecule-1 - genetics</topic><topic>Intercellular Adhesion Molecule-1 - physiology</topic><topic>intercellular adhesion molecule‐1</topic><topic>intestinal inflammation</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Other diseases. Semiology</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>ulcerative colitis adhesion molecules</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bendjelloul, F.</creatorcontrib><creatorcontrib>Malý, P.</creatorcontrib><creatorcontrib>Mandys, V.</creatorcontrib><creatorcontrib>Jirkovská, M.</creatorcontrib><creatorcontrib>Prokešová, L.</creatorcontrib><creatorcontrib>Tučková, L.</creatorcontrib><creatorcontrib>Tlaskalová‐Hogenová, H.</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>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>Bendjelloul, F.</au><au>Malý, P.</au><au>Mandys, V.</au><au>Jirkovská, M.</au><au>Prokešová, L.</au><au>Tučková, L.</au><au>Tlaskalová‐Hogenová, H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Intercellular adhesion molecule‐1 (ICAM‐1) deficiency protects mice against severe forms of experimentally induced colitis</atitle><jtitle>Clinical and experimental immunology</jtitle><addtitle>Clin Exp Immunol</addtitle><date>2000-01</date><risdate>2000</risdate><volume>119</volume><issue>1</issue><spage>57</spage><epage>63</epage><pages>57-63</pages><issn>0009-9104</issn><eissn>1365-2249</eissn><coden>CEXIAL</coden><abstract>ICAM‐1 (CD54), the ligand for LFA‐1 and Mac‐1, is up‐regulated during inflammatory reaction on the activated vascular endothelium. To determine its role in intestinal inflammation, we induced acute experimental colitis in mice with a deleted ICAM‐1 gene, by feeding them with 3% dextran sodium sulphate (DSS) in drinking water for 7 days. Chronic colitis was elicited by DSS similarly, followed by 2 weeks with water. In the acute phase of inflammation, ICAM‐1‐deficient mice exhibited a significantly lower mortality rate (5%) than control C57Bl/6J mice (35%). Control animals, but not the ICAM‐1‐deficient mice, exhibited diarrhoea and rectal bleeding. Histological examination of large‐bowel samples evaluated the intensity of inflammatory changes, and type and extent of mucosal lesions. In the acute phase, 33.3% of samples from ICAM‐1‐deficient mice exhibited mucosal defects (flat and fissural ulcers), predominantly mild to moderate inflammatory infiltrate within the lamina propria mucosae and lower grades of mucosal lesions. Much stronger inflammatory changes were present in control animals, flat ulcers (sometimes multiple) and fissural ulcers being observed in 62.5% of samples. Mucosal inflammatory infiltrate was moderate to severe, typically with higher grades of mucosal lesions. In chronic colitis, smaller inflammatory changes were found in the large bowel. The two mouse strains differed, the chronic colitis being accompanied by an increased serum level of anti‐epithelial IgA autoantibodies in C57Bl/6 control mice but not in ICAM‐1‐deficient mice. These findings provide direct evidence of the participation of ICAM‐1 molecule in the development of experimentally induced intestinal inflammation.</abstract><cop>Oxford BSL</cop><pub>Blackwell Science Ltd</pub><pmid>10606964</pmid><doi>10.1046/j.1365-2249.2000.01090.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Autoantibodies - blood Biological and medical sciences Colitis - etiology Colitis - pathology Colitis - prevention & control Dextran Sulfate - administration & dosage Dextran Sulfate - toxicity Disease Models, Animal Female Gastroenterology. Liver. Pancreas. Abdomen gene knock‐out Gut Disease Immunoglobulin A - blood Intercellular Adhesion Molecule-1 - genetics Intercellular Adhesion Molecule-1 - physiology intercellular adhesion molecule‐1 intestinal inflammation Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Other diseases. Semiology Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ulcerative colitis adhesion molecules |
| title | Intercellular adhesion molecule‐1 (ICAM‐1) deficiency protects mice against severe forms of experimentally induced colitis |
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