Galanin-1 receptor up-regulation mediates the excess colonic fluid production caused by infection with enteric pathogens
Galanin is widely distributed in enteric nerve terminals lining the gastrointestinal tract. We previously showed that pathogenic Escherichia coli, but not normal commensal organisms, increase galanin-1 receptor expression by epithelial cells lining the colon (i.e., colonocytes). When present, galani...
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| Veröffentlicht in: | Nature medicine 2000-09, Vol.6 (9), p.1048-1051 |
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| creator | Benya, Richard V Matkowskyj, Kristina A Danilkovich, Alexey Marrero, Jorge Savkovic, Suzana D Hecht, Gail |
| description | Galanin is widely distributed in enteric nerve terminals lining the gastrointestinal tract. We previously showed that pathogenic Escherichia coli, but not normal commensal organisms, increase galanin-1 receptor expression by epithelial cells lining the colon (i.e., colonocytes). When present, galanin-1 receptor activation by ligand causes colonocyte Cl- secretion. We herein demonstrate that disparate pathogens including Salmonella typhimurium and Shigella flexerii also increase colonocyte galanin-1 receptor expression, whose activation is responsible for a principal component of the increased colonic fluid secretion observed. Although eliminating the GAL1R gene by homologous recombination does not alter basal colonic fluid secretion, removal of one or both alleles completely attenuates the increase in fluid secretion due to infection with enteric pathogens. Galanin-1 receptor up-regulation therefore represents a novel mechanism accounting for the increased colonic fluid secretion observed in infectious diarrhea due to several different pathogens. |
| doi_str_mv | 10.1038/79563 |
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We previously showed that pathogenic Escherichia coli, but not normal commensal organisms, increase galanin-1 receptor expression by epithelial cells lining the colon (i.e., colonocytes). When present, galanin-1 receptor activation by ligand causes colonocyte Cl- secretion. We herein demonstrate that disparate pathogens including Salmonella typhimurium and Shigella flexerii also increase colonocyte galanin-1 receptor expression, whose activation is responsible for a principal component of the increased colonic fluid secretion observed. Although eliminating the GAL1R gene by homologous recombination does not alter basal colonic fluid secretion, removal of one or both alleles completely attenuates the increase in fluid secretion due to infection with enteric pathogens. Galanin-1 receptor up-regulation therefore represents a novel mechanism accounting for the increased colonic fluid secretion observed in infectious diarrhea due to several different pathogens.</description><identifier>ISSN: 1078-8956</identifier><identifier>EISSN: 1546-170X</identifier><identifier>DOI: 10.1038/79563</identifier><identifier>PMID: 10973327</identifier><language>eng</language><publisher>United States: Nature Publishing Group</publisher><subject>Animals ; Antibodies ; Body fluids ; Body Fluids - secretion ; Cell receptors ; Colon - metabolism ; E coli ; Enterobacter ; Enterobacteriaceae ; Enterobacteriaceae - pathogenicity ; Enterobacteriaceae infections ; Enterobacteriaceae Infections - metabolism ; Escherichia coli ; Gastrointestinal tract ; Health aspects ; Infections ; Intestinal Secretions - metabolism ; Ligands ; Medicine ; Mice ; Mice, Mutant Strains ; Pathogens ; Physiological aspects ; Receptors, Galanin ; Receptors, Neuropeptide - biosynthesis ; Risk factors ; Salmonella ; Salmonella typhimurium ; Salmonella typhimurium - pathogenicity ; Shigella flexneri ; Shigella flexneri - pathogenicity ; Up-Regulation</subject><ispartof>Nature medicine, 2000-09, Vol.6 (9), p.1048-1051</ispartof><rights>COPYRIGHT 2000 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Sep 2000</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4793-ed73244465322040329952d0d14eaed82d6774c7715d0849684db32a35e0910d3</citedby><cites>FETCH-LOGICAL-c4793-ed73244465322040329952d0d14eaed82d6774c7715d0849684db32a35e0910d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,2728,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10973327$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Benya, Richard V</creatorcontrib><creatorcontrib>Matkowskyj, Kristina A</creatorcontrib><creatorcontrib>Danilkovich, Alexey</creatorcontrib><creatorcontrib>Marrero, Jorge</creatorcontrib><creatorcontrib>Savkovic, Suzana D</creatorcontrib><creatorcontrib>Hecht, Gail</creatorcontrib><title>Galanin-1 receptor up-regulation mediates the excess colonic fluid production caused by infection with enteric pathogens</title><title>Nature medicine</title><addtitle>Nat Med</addtitle><description>Galanin is widely distributed in enteric nerve terminals lining the gastrointestinal tract. We previously showed that pathogenic Escherichia coli, but not normal commensal organisms, increase galanin-1 receptor expression by epithelial cells lining the colon (i.e., colonocytes). When present, galanin-1 receptor activation by ligand causes colonocyte Cl- secretion. We herein demonstrate that disparate pathogens including Salmonella typhimurium and Shigella flexerii also increase colonocyte galanin-1 receptor expression, whose activation is responsible for a principal component of the increased colonic fluid secretion observed. Although eliminating the GAL1R gene by homologous recombination does not alter basal colonic fluid secretion, removal of one or both alleles completely attenuates the increase in fluid secretion due to infection with enteric pathogens. Galanin-1 receptor up-regulation therefore represents a novel mechanism accounting for the increased colonic fluid secretion observed in infectious diarrhea due to several different pathogens.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Body fluids</subject><subject>Body Fluids - secretion</subject><subject>Cell receptors</subject><subject>Colon - metabolism</subject><subject>E coli</subject><subject>Enterobacter</subject><subject>Enterobacteriaceae</subject><subject>Enterobacteriaceae - pathogenicity</subject><subject>Enterobacteriaceae infections</subject><subject>Enterobacteriaceae Infections - metabolism</subject><subject>Escherichia coli</subject><subject>Gastrointestinal tract</subject><subject>Health aspects</subject><subject>Infections</subject><subject>Intestinal Secretions - metabolism</subject><subject>Ligands</subject><subject>Medicine</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Pathogens</subject><subject>Physiological aspects</subject><subject>Receptors, Galanin</subject><subject>Receptors, Neuropeptide - biosynthesis</subject><subject>Risk factors</subject><subject>Salmonella</subject><subject>Salmonella typhimurium</subject><subject>Salmonella typhimurium - pathogenicity</subject><subject>Shigella flexneri</subject><subject>Shigella flexneri - pathogenicity</subject><subject>Up-Regulation</subject><issn>1078-8956</issn><issn>1546-170X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqN0llr3DAQAGBTWpqj-QtFLTTQB6e6bFmPITRpIBDoRd-MVhqvFWxrq4Nu_n3ldSjZEmjRg4T8zeAZTVGcEHxGMGs-CFnV7FlxSCpel0TgH8_zGYumbPKHg-IohDuMMcOVfFkcECwFY1QcFtsrNajJTiVBHjRsovMobUoP6zSoaN2ERjBWRQgo9oBgqyEEpN3gJqtRNyRr0MY7k_QOa5UCGLS6R3bqYLn7ZWOPYIrgc8RGxd6tYQqvihedGgKcPOzHxbfLj18vPpU3t1fXF-c3peZCshKMYJRzXleMUswxo1JW1GBDOCgwDTW1EFwLQSqDGy7rhpsVo4pVgCXBhh0Xp0ve_Jc_E4TYjjZoGHLV4FJoBaU8r_qfkIi6kZywDN_-Be9c8lMuoqWUEUrELlu5oLUaoM3NcNErnQsHr3LvoLP5-pxIPhdVzf7sCZ-XgdHqJwPe7wVkE2Eb1_kBQnv95fP_29vv-_b0ke1BDbEPbkjzU4Z9-G6B2rsQPHTtxttR-fuW4HYeyXY3ktm9fmhXWuVZeqSWGczgzQImFZOHP2AascRzKt6w3wV94VQ</recordid><startdate>200009</startdate><enddate>200009</enddate><creator>Benya, Richard V</creator><creator>Matkowskyj, Kristina A</creator><creator>Danilkovich, Alexey</creator><creator>Marrero, Jorge</creator><creator>Savkovic, Suzana D</creator><creator>Hecht, Gail</creator><general>Nature Publishing Group</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>200009</creationdate><title>Galanin-1 receptor up-regulation mediates the excess colonic fluid production caused by infection with enteric pathogens</title><author>Benya, Richard V ; Matkowskyj, Kristina A ; Danilkovich, Alexey ; Marrero, Jorge ; Savkovic, Suzana D ; Hecht, Gail</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4793-ed73244465322040329952d0d14eaed82d6774c7715d0849684db32a35e0910d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Body fluids</topic><topic>Body Fluids - 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Academic</collection><jtitle>Nature medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Benya, Richard V</au><au>Matkowskyj, Kristina A</au><au>Danilkovich, Alexey</au><au>Marrero, Jorge</au><au>Savkovic, Suzana D</au><au>Hecht, Gail</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Galanin-1 receptor up-regulation mediates the excess colonic fluid production caused by infection with enteric pathogens</atitle><jtitle>Nature medicine</jtitle><addtitle>Nat Med</addtitle><date>2000-09</date><risdate>2000</risdate><volume>6</volume><issue>9</issue><spage>1048</spage><epage>1051</epage><pages>1048-1051</pages><issn>1078-8956</issn><eissn>1546-170X</eissn><abstract>Galanin is widely distributed in enteric nerve terminals lining the gastrointestinal tract. We previously showed that pathogenic Escherichia coli, but not normal commensal organisms, increase galanin-1 receptor expression by epithelial cells lining the colon (i.e., colonocytes). When present, galanin-1 receptor activation by ligand causes colonocyte Cl- secretion. We herein demonstrate that disparate pathogens including Salmonella typhimurium and Shigella flexerii also increase colonocyte galanin-1 receptor expression, whose activation is responsible for a principal component of the increased colonic fluid secretion observed. Although eliminating the GAL1R gene by homologous recombination does not alter basal colonic fluid secretion, removal of one or both alleles completely attenuates the increase in fluid secretion due to infection with enteric pathogens. Galanin-1 receptor up-regulation therefore represents a novel mechanism accounting for the increased colonic fluid secretion observed in infectious diarrhea due to several different pathogens.</abstract><cop>United States</cop><pub>Nature Publishing Group</pub><pmid>10973327</pmid><doi>10.1038/79563</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Nature medicine, 2000-09, Vol.6 (9), p.1048-1051 |
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| subjects | Animals Antibodies Body fluids Body Fluids - secretion Cell receptors Colon - metabolism E coli Enterobacter Enterobacteriaceae Enterobacteriaceae - pathogenicity Enterobacteriaceae infections Enterobacteriaceae Infections - metabolism Escherichia coli Gastrointestinal tract Health aspects Infections Intestinal Secretions - metabolism Ligands Medicine Mice Mice, Mutant Strains Pathogens Physiological aspects Receptors, Galanin Receptors, Neuropeptide - biosynthesis Risk factors Salmonella Salmonella typhimurium Salmonella typhimurium - pathogenicity Shigella flexneri Shigella flexneri - pathogenicity Up-Regulation |
| title | Galanin-1 receptor up-regulation mediates the excess colonic fluid production caused by infection with enteric pathogens |
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