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Clostridioides difficile biofilms: A mechanism of persistence in the gut?
C. difficile forms biofilms in vitro Biofilm formation by C. difficile was first reported by Donelli and colleagues where they identified the role of polymicrobial biofilms in clogging of biliary stents using confocal and field emission scanning electron microscopy [4]. Mutants deficient in stress-r...
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| Published in: | PLoS pathogens 2021-03, Vol.17 (3), p.e1009348-e1009348 |
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| description | C. difficile forms biofilms in vitro Biofilm formation by C. difficile was first reported by Donelli and colleagues where they identified the role of polymicrobial biofilms in clogging of biliary stents using confocal and field emission scanning electron microscopy [4]. Mutants deficient in stress-related proteins including the SOS response regulator, LexA, the RNA chaperone, Hfq, and the heat stress-associated chaperone, DnaK, have been associated with increased biofilm formation [8–10]. In a recent global gene expression analysis of microfermentor biofilms, several genes controlled by the SinR-like regulators CD2214 and CD2215, including pilA1, were differentially expressed in biofilms, although pilA1 appeared to contribute to biofilm/aggregate formation only in c-di-GMP overexpressing strains [12]. [...]C. difficile forms complex biofilms in vitro which involves multiple regulatory pathways and several virulence-associated proteins. Paradoxically, subinhibitory concentrations of metronidazole and vancomycin induced biofilm formation and seemingly reduced antibiotic susceptibility [5,18]. [...]it is possible that low levels of antibiotics could induce C. difficile biofilm production, thus promoting persistence and recurrence of infection. |
| doi_str_mv | 10.1371/journal.ppat.1009348 |
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Mutants deficient in stress-related proteins including the SOS response regulator, LexA, the RNA chaperone, Hfq, and the heat stress-associated chaperone, DnaK, have been associated with increased biofilm formation [8–10]. In a recent global gene expression analysis of microfermentor biofilms, several genes controlled by the SinR-like regulators CD2214 and CD2215, including pilA1, were differentially expressed in biofilms, although pilA1 appeared to contribute to biofilm/aggregate formation only in c-di-GMP overexpressing strains [12]. [...]C. difficile forms complex biofilms in vitro which involves multiple regulatory pathways and several virulence-associated proteins. Paradoxically, subinhibitory concentrations of metronidazole and vancomycin induced biofilm formation and seemingly reduced antibiotic susceptibility [5,18]. [...]it is possible that low levels of antibiotics could induce C. difficile biofilm production, thus promoting persistence and recurrence of infection.</description><identifier>ISSN: 1553-7374</identifier><identifier>ISSN: 1553-7366</identifier><identifier>EISSN: 1553-7374</identifier><identifier>DOI: 10.1371/journal.ppat.1009348</identifier><identifier>PMID: 33705497</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Antibiotics ; Antimicrobial agents ; Biofilms ; Biology and Life Sciences ; Clostridium difficile ; Clostridium infections ; Development and progression ; Digestive organs ; DnaK protein ; Drug resistance ; Field emission microscopy ; Gene expression ; Health aspects ; Heat stress ; Heat tolerance ; Implants ; Infections ; Medicine and Health Sciences ; Metronidazole ; Microbial mats ; Microbiota ; Pearls ; Physiological aspects ; Proteins ; Research and Analysis Methods ; Scanning electron microscopy ; SOS response ; Vancomycin ; Virulence</subject><ispartof>PLoS pathogens, 2021-03, Vol.17 (3), p.e1009348-e1009348</ispartof><rights>COPYRIGHT 2021 Public Library of Science</rights><rights>2021 Frost et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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Mutants deficient in stress-related proteins including the SOS response regulator, LexA, the RNA chaperone, Hfq, and the heat stress-associated chaperone, DnaK, have been associated with increased biofilm formation [8–10]. In a recent global gene expression analysis of microfermentor biofilms, several genes controlled by the SinR-like regulators CD2214 and CD2215, including pilA1, were differentially expressed in biofilms, although pilA1 appeared to contribute to biofilm/aggregate formation only in c-di-GMP overexpressing strains [12]. [...]C. difficile forms complex biofilms in vitro which involves multiple regulatory pathways and several virulence-associated proteins. Paradoxically, subinhibitory concentrations of metronidazole and vancomycin induced biofilm formation and seemingly reduced antibiotic susceptibility [5,18]. [...]it is possible that low levels of antibiotics could induce C. difficile biofilm production, thus promoting persistence and recurrence of infection.</description><subject>Antibiotics</subject><subject>Antimicrobial agents</subject><subject>Biofilms</subject><subject>Biology and Life Sciences</subject><subject>Clostridium difficile</subject><subject>Clostridium infections</subject><subject>Development and progression</subject><subject>Digestive organs</subject><subject>DnaK protein</subject><subject>Drug resistance</subject><subject>Field emission microscopy</subject><subject>Gene expression</subject><subject>Health aspects</subject><subject>Heat stress</subject><subject>Heat tolerance</subject><subject>Implants</subject><subject>Infections</subject><subject>Medicine and Health Sciences</subject><subject>Metronidazole</subject><subject>Microbial mats</subject><subject>Microbiota</subject><subject>Pearls</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Research and Analysis Methods</subject><subject>Scanning electron microscopy</subject><subject>SOS response</subject><subject>Vancomycin</subject><subject>Virulence</subject><issn>1553-7374</issn><issn>1553-7366</issn><issn>1553-7374</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNqVkk2P0zAQhiMEYpeFf4AgEhc4tNjxV8wBVFV8VFqBxMfZcuxx6yqJu3aC4N_j0Oxqi_aCfLBlP_POvOMpiqcYLTER-PU-jLHX7fJw0MMSIyQJre8V55gxshBE0Pu3zmfFo5T2CFFMMH9YnBEiEKNSnBebdRvSEL31wVtIpfXOeeNbKBsfnG-79KZclR2Yne596srgygPE5NMAvYHS9-Wwg3I7Du8eFw-cbhM8mfeL4seH99_XnxaXXz5u1qvLheEcDwtbcYclYg0BZCxGlXNUNpjjqhFWUKd5vnSccood1AIqBq7RtQFrcS2YIBfF86PuIVeu5i4kVTFMeC0lZZnYHAkb9F4dou90_K2C9urvRYhbpePgTQuKA4hGYudILoNaJ6tK2AbhGhEpmUZZ6-2cbWw6sAb6Ier2RPT0pfc7tQ0_lZAs26RZ4OUsEMPVCGlQnU8G2lb3EMapboSr7L6acr34B73b3UxtdTbgexdyXjOJqhVntcCYo0lreQeVl4XOm9BD_ls4DXh1EpCZAX4NWz2mpDbfvv4H-_mUpUfWxJBSBHfTO4zUNMjXJtU0yGoe5Bz27Hbfb4KuJ5f8AblZ7ag</recordid><startdate>20210301</startdate><enddate>20210301</enddate><creator>Frost, Lucy R</creator><creator>Cheng, Jeffrey K J</creator><creator>Unnikrishnan, Meera</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>ISN</scope><scope>ISR</scope><scope>3V.</scope><scope>7QL</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-0750-778X</orcidid><orcidid>https://orcid.org/0000-0002-4093-7872</orcidid><orcidid>https://orcid.org/0000-0001-5417-9331</orcidid></search><sort><creationdate>20210301</creationdate><title>Clostridioides difficile biofilms: A mechanism of persistence in the gut?</title><author>Frost, Lucy R ; Cheng, Jeffrey K J ; Unnikrishnan, Meera</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c661t-d26f1905b3e0cd102ff49b1612b7d74fa6d10f64641fe87e25efba8cedd187573</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Antibiotics</topic><topic>Antimicrobial agents</topic><topic>Biofilms</topic><topic>Biology and Life Sciences</topic><topic>Clostridium difficile</topic><topic>Clostridium infections</topic><topic>Development and progression</topic><topic>Digestive organs</topic><topic>DnaK protein</topic><topic>Drug resistance</topic><topic>Field emission microscopy</topic><topic>Gene expression</topic><topic>Health aspects</topic><topic>Heat stress</topic><topic>Heat tolerance</topic><topic>Implants</topic><topic>Infections</topic><topic>Medicine and Health Sciences</topic><topic>Metronidazole</topic><topic>Microbial mats</topic><topic>Microbiota</topic><topic>Pearls</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>Research and Analysis Methods</topic><topic>Scanning electron microscopy</topic><topic>SOS response</topic><topic>Vancomycin</topic><topic>Virulence</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Frost, Lucy R</creatorcontrib><creatorcontrib>Cheng, Jeffrey K J</creatorcontrib><creatorcontrib>Unnikrishnan, Meera</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Canada</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Virology and AIDS Abstracts</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</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>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Biological Science Journals</collection><collection>Publicly Available Content (ProQuest)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PLoS pathogens</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Frost, Lucy R</au><au>Cheng, Jeffrey K J</au><au>Unnikrishnan, Meera</au><au>Hogan, Deborah A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Clostridioides difficile biofilms: A mechanism of persistence in the gut?</atitle><jtitle>PLoS pathogens</jtitle><addtitle>PLoS Pathog</addtitle><date>2021-03-01</date><risdate>2021</risdate><volume>17</volume><issue>3</issue><spage>e1009348</spage><epage>e1009348</epage><pages>e1009348-e1009348</pages><issn>1553-7374</issn><issn>1553-7366</issn><eissn>1553-7374</eissn><abstract>C. difficile forms biofilms in vitro Biofilm formation by C. difficile was first reported by Donelli and colleagues where they identified the role of polymicrobial biofilms in clogging of biliary stents using confocal and field emission scanning electron microscopy [4]. 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| subjects | Antibiotics Antimicrobial agents Biofilms Biology and Life Sciences Clostridium difficile Clostridium infections Development and progression Digestive organs DnaK protein Drug resistance Field emission microscopy Gene expression Health aspects Heat stress Heat tolerance Implants Infections Medicine and Health Sciences Metronidazole Microbial mats Microbiota Pearls Physiological aspects Proteins Research and Analysis Methods Scanning electron microscopy SOS response Vancomycin Virulence |
| title | Clostridioides difficile biofilms: A mechanism of persistence in the gut? |
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