Role of Enterococcus faecalis surface protein Esp in the pathogenesis of ascending urinary tract infection
Enterococcus faecalis bacteria isolated from patients with bacteremia, endocarditis, and urinary tract infections more frequently express the surface protein Esp than do fecal isolates. To assess the role of Esp in colonization and persistence of E. faecalis in an animal model of ascending urinary t...
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Veröffentlicht in: | Infection and immunity 2001-07, Vol.69 (7), p.4366-4372 |
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description | Enterococcus faecalis bacteria isolated from patients with bacteremia, endocarditis, and urinary tract infections more frequently express the surface protein Esp than do fecal isolates. To assess the role of Esp in colonization and persistence of E. faecalis in an animal model of ascending urinary tract infection, we compared an Esp(+) strain of E. faecalis to its isogenic Esp-deficient mutant. Groups of CBA/J mice were challenged transurethrally with 10(8) CFU of either the parent or mutant strain, and bacteria in the urine, bladder, and kidneys were enumerated 5 days postinfection. Significantly higher numbers of bacteria were recovered from the bladder and urine of mice challenged with the parent strain than from the bladder and urine of mice challenged with the mutant. Colonization of the kidney, however, was not significantly different between the parent and mutant strains. Histopathological evaluations of kidney and bladder tissue done at 5 days postinfection did not show marked histopathological changes consistent with inflammation, mucosal hyperplasia, or apoptosis, and there was no observable difference between the mice challenged with the parent and those challenged with the mutant. We conclude that, while Esp does not influence histopathological changes associated with acute urinary tract infections, it contributes to colonization and persistence of E. faecalis at this site. |
doi_str_mv | 10.1128/IAI.69.7.4366-4372.2001 |
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Virginia ; BAGHDAYAN, Arto S ; DRACHENBERG, C ; GILMORE, Michael S ; JOHNSON, David E</creator><contributor>Tuomanen, E. I.</contributor><creatorcontrib>SHANKAR, Nathan ; LOCKATELL, C. Virginia ; BAGHDAYAN, Arto S ; DRACHENBERG, C ; GILMORE, Michael S ; JOHNSON, David E ; Tuomanen, E. I.</creatorcontrib><description>Enterococcus faecalis bacteria isolated from patients with bacteremia, endocarditis, and urinary tract infections more frequently express the surface protein Esp than do fecal isolates. To assess the role of Esp in colonization and persistence of E. faecalis in an animal model of ascending urinary tract infection, we compared an Esp(+) strain of E. faecalis to its isogenic Esp-deficient mutant. Groups of CBA/J mice were challenged transurethrally with 10(8) CFU of either the parent or mutant strain, and bacteria in the urine, bladder, and kidneys were enumerated 5 days postinfection. Significantly higher numbers of bacteria were recovered from the bladder and urine of mice challenged with the parent strain than from the bladder and urine of mice challenged with the mutant. Colonization of the kidney, however, was not significantly different between the parent and mutant strains. Histopathological evaluations of kidney and bladder tissue done at 5 days postinfection did not show marked histopathological changes consistent with inflammation, mucosal hyperplasia, or apoptosis, and there was no observable difference between the mice challenged with the parent and those challenged with the mutant. We conclude that, while Esp does not influence histopathological changes associated with acute urinary tract infections, it contributes to colonization and persistence of E. faecalis at this site.</description><identifier>ISSN: 0019-9567</identifier><identifier>EISSN: 1098-5522</identifier><identifier>DOI: 10.1128/IAI.69.7.4366-4372.2001</identifier><identifier>PMID: 11401975</identifier><identifier>CODEN: INFIBR</identifier><language>eng</language><publisher>Washington, DC: American Society for Microbiology</publisher><subject>Animals ; Bacterial diseases ; Bacterial Infections ; Bacterial Proteins - genetics ; Bacterial Proteins - physiology ; Biological and medical sciences ; Disease Models, Animal ; Enterococcus faecalis ; Enterococcus faecalis - genetics ; Enterococcus faecalis - pathogenicity ; Esp protein ; Experimental bacterial diseases and models ; Experimental protozoal diseases and models ; Fundamental and applied biological sciences. Psychology ; Gram-Positive Bacterial Infections - microbiology ; Humans ; Infectious diseases ; Medical sciences ; Membrane Proteins - genetics ; Membrane Proteins - physiology ; Mice ; Mice, Inbred CBA ; Microbiology ; Parasitic diseases ; Phenotype ; Protozoal diseases ; Rabbits ; Urinary Tract Infections - microbiology</subject><ispartof>Infection and immunity, 2001-07, Vol.69 (7), p.4366-4372</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright © 2001, American Society for Microbiology 2001</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c472t-1b23818771b124a76a618da9ca45730554ffa64892c26a551189f4311b04add83</citedby><cites>FETCH-LOGICAL-c472t-1b23818771b124a76a618da9ca45730554ffa64892c26a551189f4311b04add83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC98508/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC98508/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,3186,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14162142$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11401975$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Tuomanen, E. I.</contributor><creatorcontrib>SHANKAR, Nathan</creatorcontrib><creatorcontrib>LOCKATELL, C. Virginia</creatorcontrib><creatorcontrib>BAGHDAYAN, Arto S</creatorcontrib><creatorcontrib>DRACHENBERG, C</creatorcontrib><creatorcontrib>GILMORE, Michael S</creatorcontrib><creatorcontrib>JOHNSON, David E</creatorcontrib><title>Role of Enterococcus faecalis surface protein Esp in the pathogenesis of ascending urinary tract infection</title><title>Infection and immunity</title><addtitle>Infect Immun</addtitle><description>Enterococcus faecalis bacteria isolated from patients with bacteremia, endocarditis, and urinary tract infections more frequently express the surface protein Esp than do fecal isolates. To assess the role of Esp in colonization and persistence of E. faecalis in an animal model of ascending urinary tract infection, we compared an Esp(+) strain of E. faecalis to its isogenic Esp-deficient mutant. Groups of CBA/J mice were challenged transurethrally with 10(8) CFU of either the parent or mutant strain, and bacteria in the urine, bladder, and kidneys were enumerated 5 days postinfection. Significantly higher numbers of bacteria were recovered from the bladder and urine of mice challenged with the parent strain than from the bladder and urine of mice challenged with the mutant. Colonization of the kidney, however, was not significantly different between the parent and mutant strains. Histopathological evaluations of kidney and bladder tissue done at 5 days postinfection did not show marked histopathological changes consistent with inflammation, mucosal hyperplasia, or apoptosis, and there was no observable difference between the mice challenged with the parent and those challenged with the mutant. We conclude that, while Esp does not influence histopathological changes associated with acute urinary tract infections, it contributes to colonization and persistence of E. faecalis at this site.</description><subject>Animals</subject><subject>Bacterial diseases</subject><subject>Bacterial Infections</subject><subject>Bacterial Proteins - genetics</subject><subject>Bacterial Proteins - physiology</subject><subject>Biological and medical sciences</subject><subject>Disease Models, Animal</subject><subject>Enterococcus faecalis</subject><subject>Enterococcus faecalis - genetics</subject><subject>Enterococcus faecalis - pathogenicity</subject><subject>Esp protein</subject><subject>Experimental bacterial diseases and models</subject><subject>Experimental protozoal diseases and models</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gram-Positive Bacterial Infections - microbiology</subject><subject>Humans</subject><subject>Infectious diseases</subject><subject>Medical sciences</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - physiology</subject><subject>Mice</subject><subject>Mice, Inbred CBA</subject><subject>Microbiology</subject><subject>Parasitic diseases</subject><subject>Phenotype</subject><subject>Protozoal diseases</subject><subject>Rabbits</subject><subject>Urinary Tract Infections - microbiology</subject><issn>0019-9567</issn><issn>1098-5522</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU-LFDEQxYMo7rj6FTQXvXWbSucveFmWUQcWBNFzyKSTmSw9yZh0C3570-zg6slTkarfK17lIfQGSA9A1fvdza4Xupc9G4To2CBpTwmBJ2gDRKuOc0qfok3r6E5zIa_Qi1rv25Mxpp6jKwDWRpJv0P3XPHmcA96m2ZfssnNLxcF6Z6dYcV1KsM7jc8mzjwlv6xm3Mh9by87HfPDJ18a1BbY6n8aYDngpMdnyC8_Furnhwbs55vQSPQt2qv7VpV6j7x-3324_d3dfPu1ub-46xySdO9jTQYGSEvZAmZXCClCj1c4yLgfCOQvBCqY0dVRYzgGUDmwA2BNmx1EN1-jDw97zsj_5sblqRiZzLvHUXJlso_l3kuLRHPJPoxUnq_zdRV7yj8XX2ZxiO22abPJ5qUYSTaVU4r8gKCKHgbMGygfQlVxr8eGPFyBmjdO0OI3QRpo1TrPGadY4m_L136c86i75NeDtBWjfb6dQbHKxPnIMBAVGh994Fapm</recordid><startdate>20010701</startdate><enddate>20010701</enddate><creator>SHANKAR, Nathan</creator><creator>LOCKATELL, C. 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Virginia ; BAGHDAYAN, Arto S ; DRACHENBERG, C ; GILMORE, Michael S ; JOHNSON, David E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c472t-1b23818771b124a76a618da9ca45730554ffa64892c26a551189f4311b04add83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Bacterial diseases</topic><topic>Bacterial Infections</topic><topic>Bacterial Proteins - genetics</topic><topic>Bacterial Proteins - physiology</topic><topic>Biological and medical sciences</topic><topic>Disease Models, Animal</topic><topic>Enterococcus faecalis</topic><topic>Enterococcus faecalis - genetics</topic><topic>Enterococcus faecalis - pathogenicity</topic><topic>Esp protein</topic><topic>Experimental bacterial diseases and models</topic><topic>Experimental protozoal diseases and models</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gram-Positive Bacterial Infections - microbiology</topic><topic>Humans</topic><topic>Infectious diseases</topic><topic>Medical sciences</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - physiology</topic><topic>Mice</topic><topic>Mice, Inbred CBA</topic><topic>Microbiology</topic><topic>Parasitic diseases</topic><topic>Phenotype</topic><topic>Protozoal diseases</topic><topic>Rabbits</topic><topic>Urinary Tract Infections - microbiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SHANKAR, Nathan</creatorcontrib><creatorcontrib>LOCKATELL, C. Virginia</creatorcontrib><creatorcontrib>BAGHDAYAN, Arto S</creatorcontrib><creatorcontrib>DRACHENBERG, C</creatorcontrib><creatorcontrib>GILMORE, Michael S</creatorcontrib><creatorcontrib>JOHNSON, David E</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Infection and immunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SHANKAR, Nathan</au><au>LOCKATELL, C. Virginia</au><au>BAGHDAYAN, Arto S</au><au>DRACHENBERG, C</au><au>GILMORE, Michael S</au><au>JOHNSON, David E</au><au>Tuomanen, E. I.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of Enterococcus faecalis surface protein Esp in the pathogenesis of ascending urinary tract infection</atitle><jtitle>Infection and immunity</jtitle><addtitle>Infect Immun</addtitle><date>2001-07-01</date><risdate>2001</risdate><volume>69</volume><issue>7</issue><spage>4366</spage><epage>4372</epage><pages>4366-4372</pages><issn>0019-9567</issn><eissn>1098-5522</eissn><coden>INFIBR</coden><abstract>Enterococcus faecalis bacteria isolated from patients with bacteremia, endocarditis, and urinary tract infections more frequently express the surface protein Esp than do fecal isolates. To assess the role of Esp in colonization and persistence of E. faecalis in an animal model of ascending urinary tract infection, we compared an Esp(+) strain of E. faecalis to its isogenic Esp-deficient mutant. Groups of CBA/J mice were challenged transurethrally with 10(8) CFU of either the parent or mutant strain, and bacteria in the urine, bladder, and kidneys were enumerated 5 days postinfection. Significantly higher numbers of bacteria were recovered from the bladder and urine of mice challenged with the parent strain than from the bladder and urine of mice challenged with the mutant. Colonization of the kidney, however, was not significantly different between the parent and mutant strains. Histopathological evaluations of kidney and bladder tissue done at 5 days postinfection did not show marked histopathological changes consistent with inflammation, mucosal hyperplasia, or apoptosis, and there was no observable difference between the mice challenged with the parent and those challenged with the mutant. We conclude that, while Esp does not influence histopathological changes associated with acute urinary tract infections, it contributes to colonization and persistence of E. faecalis at this site.</abstract><cop>Washington, DC</cop><pub>American Society for Microbiology</pub><pmid>11401975</pmid><doi>10.1128/IAI.69.7.4366-4372.2001</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Bacterial diseases Bacterial Infections Bacterial Proteins - genetics Bacterial Proteins - physiology Biological and medical sciences Disease Models, Animal Enterococcus faecalis Enterococcus faecalis - genetics Enterococcus faecalis - pathogenicity Esp protein Experimental bacterial diseases and models Experimental protozoal diseases and models Fundamental and applied biological sciences. Psychology Gram-Positive Bacterial Infections - microbiology Humans Infectious diseases Medical sciences Membrane Proteins - genetics Membrane Proteins - physiology Mice Mice, Inbred CBA Microbiology Parasitic diseases Phenotype Protozoal diseases Rabbits Urinary Tract Infections - microbiology |
title | Role of Enterococcus faecalis surface protein Esp in the pathogenesis of ascending urinary tract infection |
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