Remodeling of the Candida glabrata cell wall in the gastrointestinal tract affects the gut microbiota and the immune response
The gastrointestinal (GI) microbiota acts a natural barrier to the proliferation of opportunistic pathogens. Candida glabrata is an opportunistic yeast pathogen that has adapted to colonize all segments of the human GI tract. We observed an increase in Escherichia coli , Enterococcus faecalis , and...
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| Veröffentlicht in: | Scientific reports 2018-02, Vol.8 (1), p.3316-12, Article 3316 |
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| creator | Charlet, Rogatien Pruvost, Youri Tumba, Gael Istel, Fabian Poulain, Daniel Kuchler, Karl Sendid, Boualem Jawhara, Samir |
| description | The gastrointestinal (GI) microbiota acts a natural barrier to the proliferation of opportunistic pathogens.
Candida glabrata
is an opportunistic yeast pathogen that has adapted to colonize all segments of the human GI tract. We observed an increase in
Escherichia coli
,
Enterococcus faecalis
, and
Bacteroides vulgatus
populations, and a decrease in
Lactobacillus johnsonii
,
Bacteroides thetaiotaomicron
, and
Bifidobacterium animalis
in mice with DSS-induced colitis. This reduction was more pronounced for
L. johnsonii
during
C. glabrata
overgrowth. In addition,
C. glabrata
overgrowth increased mouse mortality and inflammatory parameters, and modulated the expression of intestinal receptors and signaling pathways. The
C. glabrata
cell wall underwent various changes during the course of
C. glabrata
colonization, and showed a significant increase in chitin.
C. glabrata
deficient in chitin synthase-3 induced fewer inflammatory parameters than the parental strain during intestinal inflammation. Oral administration of chitin attenuated the impact of colitis, and reduced the number of aerobic bacteria and
C. glabrata
overgrowth, while chitinase-3-like protein-1 increased. This study provides evidence that inflammation of the gut alters the microbial balance and leads to
C. glabrata
cell wall remodeling through an increase in chitin, which is involved in promoting persistence of
C. glabrata
in the gut. |
| doi_str_mv | 10.1038/s41598-018-21422-w |
| format | Article |
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Candida glabrata
is an opportunistic yeast pathogen that has adapted to colonize all segments of the human GI tract. We observed an increase in
Escherichia coli
,
Enterococcus faecalis
, and
Bacteroides vulgatus
populations, and a decrease in
Lactobacillus johnsonii
,
Bacteroides thetaiotaomicron
, and
Bifidobacterium animalis
in mice with DSS-induced colitis. This reduction was more pronounced for
L. johnsonii
during
C. glabrata
overgrowth. In addition,
C. glabrata
overgrowth increased mouse mortality and inflammatory parameters, and modulated the expression of intestinal receptors and signaling pathways. The
C. glabrata
cell wall underwent various changes during the course of
C. glabrata
colonization, and showed a significant increase in chitin.
C. glabrata
deficient in chitin synthase-3 induced fewer inflammatory parameters than the parental strain during intestinal inflammation. Oral administration of chitin attenuated the impact of colitis, and reduced the number of aerobic bacteria and
C. glabrata
overgrowth, while chitinase-3-like protein-1 increased. This study provides evidence that inflammation of the gut alters the microbial balance and leads to
C. glabrata
cell wall remodeling through an increase in chitin, which is involved in promoting persistence of
C. glabrata
in the gut.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-018-21422-w</identifier><identifier>PMID: 29463799</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/21 ; 13/31 ; 13/51 ; 42/34 ; 692/4020/1503/2745 ; 692/699/255/1672 ; 82/80 ; 96/1 ; 96/63 ; Aerobic bacteria ; Animals ; Bacteroides ; Candida glabrata ; Candida glabrata - growth & development ; Candida glabrata - immunology ; Candida glabrata - pathogenicity ; Candidiasis - immunology ; Candidiasis - microbiology ; Cell Wall - immunology ; Cell Wall - microbiology ; Cell walls ; Chitin ; Chitin synthase ; Chitinase ; Colitis ; Colitis - chemically induced ; Colitis - immunology ; Colitis - microbiology ; Colonization ; Dextran Sulfate - toxicity ; Digestive system ; E coli ; Female ; Gastrointestinal Microbiome - immunology ; Gastrointestinal tract ; Gastrointestinal Tract - immunology ; Gastrointestinal Tract - microbiology ; Humanities and Social Sciences ; Immune response ; Inflammation ; Inflammation - etiology ; Inflammation - pathology ; Inflammatory bowel disease ; Intestinal microflora ; Intestine ; Intestines - immunology ; Intestines - microbiology ; Life Sciences ; Mice ; Mice, Inbred C57BL ; Microbiota ; multidisciplinary ; Opportunist infection ; Oral administration ; Pathogens ; Science ; Science (multidisciplinary) ; Yeasts</subject><ispartof>Scientific reports, 2018-02, Vol.8 (1), p.3316-12, Article 3316</ispartof><rights>The Author(s) 2018</rights><rights>2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Attribution</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c508t-d9e3f5e49a4b926a259a648a7d5f6740814362f59d9eaaa4d51c060829b0acc53</citedby><cites>FETCH-LOGICAL-c508t-d9e3f5e49a4b926a259a648a7d5f6740814362f59d9eaaa4d51c060829b0acc53</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/PMC5820338/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5820338/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29463799$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.univ-lille.fr/hal-04490843$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Charlet, Rogatien</creatorcontrib><creatorcontrib>Pruvost, Youri</creatorcontrib><creatorcontrib>Tumba, Gael</creatorcontrib><creatorcontrib>Istel, Fabian</creatorcontrib><creatorcontrib>Poulain, Daniel</creatorcontrib><creatorcontrib>Kuchler, Karl</creatorcontrib><creatorcontrib>Sendid, Boualem</creatorcontrib><creatorcontrib>Jawhara, Samir</creatorcontrib><title>Remodeling of the Candida glabrata cell wall in the gastrointestinal tract affects the gut microbiota and the immune response</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>The gastrointestinal (GI) microbiota acts a natural barrier to the proliferation of opportunistic pathogens.
Candida glabrata
is an opportunistic yeast pathogen that has adapted to colonize all segments of the human GI tract. We observed an increase in
Escherichia coli
,
Enterococcus faecalis
, and
Bacteroides vulgatus
populations, and a decrease in
Lactobacillus johnsonii
,
Bacteroides thetaiotaomicron
, and
Bifidobacterium animalis
in mice with DSS-induced colitis. This reduction was more pronounced for
L. johnsonii
during
C. glabrata
overgrowth. In addition,
C. glabrata
overgrowth increased mouse mortality and inflammatory parameters, and modulated the expression of intestinal receptors and signaling pathways. The
C. glabrata
cell wall underwent various changes during the course of
C. glabrata
colonization, and showed a significant increase in chitin.
C. glabrata
deficient in chitin synthase-3 induced fewer inflammatory parameters than the parental strain during intestinal inflammation. Oral administration of chitin attenuated the impact of colitis, and reduced the number of aerobic bacteria and
C. glabrata
overgrowth, while chitinase-3-like protein-1 increased. This study provides evidence that inflammation of the gut alters the microbial balance and leads to
C. glabrata
cell wall remodeling through an increase in chitin, which is involved in promoting persistence of
C. glabrata
in the gut.</description><subject>13/21</subject><subject>13/31</subject><subject>13/51</subject><subject>42/34</subject><subject>692/4020/1503/2745</subject><subject>692/699/255/1672</subject><subject>82/80</subject><subject>96/1</subject><subject>96/63</subject><subject>Aerobic bacteria</subject><subject>Animals</subject><subject>Bacteroides</subject><subject>Candida glabrata</subject><subject>Candida glabrata - growth & development</subject><subject>Candida glabrata - immunology</subject><subject>Candida glabrata - pathogenicity</subject><subject>Candidiasis - immunology</subject><subject>Candidiasis - microbiology</subject><subject>Cell Wall - immunology</subject><subject>Cell Wall - microbiology</subject><subject>Cell walls</subject><subject>Chitin</subject><subject>Chitin synthase</subject><subject>Chitinase</subject><subject>Colitis</subject><subject>Colitis - chemically induced</subject><subject>Colitis - immunology</subject><subject>Colitis - microbiology</subject><subject>Colonization</subject><subject>Dextran Sulfate - toxicity</subject><subject>Digestive system</subject><subject>E coli</subject><subject>Female</subject><subject>Gastrointestinal Microbiome - immunology</subject><subject>Gastrointestinal tract</subject><subject>Gastrointestinal Tract - immunology</subject><subject>Gastrointestinal Tract - microbiology</subject><subject>Humanities and Social Sciences</subject><subject>Immune response</subject><subject>Inflammation</subject><subject>Inflammation - etiology</subject><subject>Inflammation - pathology</subject><subject>Inflammatory bowel disease</subject><subject>Intestinal microflora</subject><subject>Intestine</subject><subject>Intestines - immunology</subject><subject>Intestines - microbiology</subject><subject>Life Sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microbiota</subject><subject>multidisciplinary</subject><subject>Opportunist infection</subject><subject>Oral administration</subject><subject>Pathogens</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Yeasts</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kk1r3DAQhk1paUKSP9BDEfTSHpzo05YuhbA0H7BQKO1ZjG3Zq2BLW0nOkkP_e7XrNE1zqA6SmHnmndFoiuIdwecEM3kRORFKlpjIkhJOabl7VRxTzEVJGaWvn92PirMY73BegipO1NviKJ8Vq5U6Ln59M5PvzGjdgHyP0sagFbjOdoCGEZoACVBrxhHtIG_WHYgBYgreumRisg5GlAK0CUHfmzbFBZkTmmwbfGN9lsiSB7OdptkZFEzcehfNafGmhzGas8fzpPhx9eX76qZcf72-XV2uy1ZgmcpOGdYLwxXwRtEKqFBQcQl1J_qq5lgSziraC5VBAOCdIC2usKSqwdC2gp0Unxfd7dxMpmuNyxWPehvsBOFBe7D6X4-zGz34ey0kxYzJLPBpEdi8CLu5XOu9DXOusOTsnmT242Oy4H_OuUV6snHfQ3DGz1FTjGtCqlpUGf3wAr3zc8gdPVCVJILxOlN0oXI7Ywymf6qAYL0fBr0Mg87DoA_DoHc56P3zJz-F_Pn6DLAFiNnlBhP-5v6P7G8vgMEz</recordid><startdate>20180220</startdate><enddate>20180220</enddate><creator>Charlet, Rogatien</creator><creator>Pruvost, Youri</creator><creator>Tumba, Gael</creator><creator>Istel, Fabian</creator><creator>Poulain, Daniel</creator><creator>Kuchler, Karl</creator><creator>Sendid, Boualem</creator><creator>Jawhara, Samir</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope></search><sort><creationdate>20180220</creationdate><title>Remodeling of the Candida glabrata cell wall in the gastrointestinal tract affects the gut microbiota and the immune response</title><author>Charlet, Rogatien ; Pruvost, Youri ; Tumba, Gael ; Istel, Fabian ; Poulain, Daniel ; Kuchler, Karl ; Sendid, Boualem ; Jawhara, Samir</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c508t-d9e3f5e49a4b926a259a648a7d5f6740814362f59d9eaaa4d51c060829b0acc53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>13/21</topic><topic>13/31</topic><topic>13/51</topic><topic>42/34</topic><topic>692/4020/1503/2745</topic><topic>692/699/255/1672</topic><topic>82/80</topic><topic>96/1</topic><topic>96/63</topic><topic>Aerobic bacteria</topic><topic>Animals</topic><topic>Bacteroides</topic><topic>Candida glabrata</topic><topic>Candida glabrata - growth & development</topic><topic>Candida glabrata - immunology</topic><topic>Candida glabrata - pathogenicity</topic><topic>Candidiasis - immunology</topic><topic>Candidiasis - microbiology</topic><topic>Cell Wall - immunology</topic><topic>Cell Wall - microbiology</topic><topic>Cell walls</topic><topic>Chitin</topic><topic>Chitin synthase</topic><topic>Chitinase</topic><topic>Colitis</topic><topic>Colitis - chemically induced</topic><topic>Colitis - immunology</topic><topic>Colitis - microbiology</topic><topic>Colonization</topic><topic>Dextran Sulfate - toxicity</topic><topic>Digestive system</topic><topic>E coli</topic><topic>Female</topic><topic>Gastrointestinal Microbiome - immunology</topic><topic>Gastrointestinal tract</topic><topic>Gastrointestinal Tract - immunology</topic><topic>Gastrointestinal Tract - microbiology</topic><topic>Humanities and Social Sciences</topic><topic>Immune response</topic><topic>Inflammation</topic><topic>Inflammation - etiology</topic><topic>Inflammation - pathology</topic><topic>Inflammatory bowel disease</topic><topic>Intestinal microflora</topic><topic>Intestine</topic><topic>Intestines - immunology</topic><topic>Intestines - microbiology</topic><topic>Life Sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Microbiota</topic><topic>multidisciplinary</topic><topic>Opportunist infection</topic><topic>Oral administration</topic><topic>Pathogens</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Yeasts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Charlet, Rogatien</creatorcontrib><creatorcontrib>Pruvost, Youri</creatorcontrib><creatorcontrib>Tumba, Gael</creatorcontrib><creatorcontrib>Istel, Fabian</creatorcontrib><creatorcontrib>Poulain, Daniel</creatorcontrib><creatorcontrib>Kuchler, Karl</creatorcontrib><creatorcontrib>Sendid, Boualem</creatorcontrib><creatorcontrib>Jawhara, Samir</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science 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 Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</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>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</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 Basic</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Charlet, Rogatien</au><au>Pruvost, Youri</au><au>Tumba, Gael</au><au>Istel, Fabian</au><au>Poulain, Daniel</au><au>Kuchler, Karl</au><au>Sendid, Boualem</au><au>Jawhara, Samir</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Remodeling of the Candida glabrata cell wall in the gastrointestinal tract affects the gut microbiota and the immune response</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2018-02-20</date><risdate>2018</risdate><volume>8</volume><issue>1</issue><spage>3316</spage><epage>12</epage><pages>3316-12</pages><artnum>3316</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>The gastrointestinal (GI) microbiota acts a natural barrier to the proliferation of opportunistic pathogens.
Candida glabrata
is an opportunistic yeast pathogen that has adapted to colonize all segments of the human GI tract. We observed an increase in
Escherichia coli
,
Enterococcus faecalis
, and
Bacteroides vulgatus
populations, and a decrease in
Lactobacillus johnsonii
,
Bacteroides thetaiotaomicron
, and
Bifidobacterium animalis
in mice with DSS-induced colitis. This reduction was more pronounced for
L. johnsonii
during
C. glabrata
overgrowth. In addition,
C. glabrata
overgrowth increased mouse mortality and inflammatory parameters, and modulated the expression of intestinal receptors and signaling pathways. The
C. glabrata
cell wall underwent various changes during the course of
C. glabrata
colonization, and showed a significant increase in chitin.
C. glabrata
deficient in chitin synthase-3 induced fewer inflammatory parameters than the parental strain during intestinal inflammation. Oral administration of chitin attenuated the impact of colitis, and reduced the number of aerobic bacteria and
C. glabrata
overgrowth, while chitinase-3-like protein-1 increased. This study provides evidence that inflammation of the gut alters the microbial balance and leads to
C. glabrata
cell wall remodeling through an increase in chitin, which is involved in promoting persistence of
C. glabrata
in the gut.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29463799</pmid><doi>10.1038/s41598-018-21422-w</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | Scientific reports, 2018-02, Vol.8 (1), p.3316-12, Article 3316 |
| issn | 2045-2322 2045-2322 |
| language | eng |
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| source | MEDLINE; Nature Free; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry; Springer Nature OA Free Journals |
| subjects | 13/21 13/31 13/51 42/34 692/4020/1503/2745 692/699/255/1672 82/80 96/1 96/63 Aerobic bacteria Animals Bacteroides Candida glabrata Candida glabrata - growth & development Candida glabrata - immunology Candida glabrata - pathogenicity Candidiasis - immunology Candidiasis - microbiology Cell Wall - immunology Cell Wall - microbiology Cell walls Chitin Chitin synthase Chitinase Colitis Colitis - chemically induced Colitis - immunology Colitis - microbiology Colonization Dextran Sulfate - toxicity Digestive system E coli Female Gastrointestinal Microbiome - immunology Gastrointestinal tract Gastrointestinal Tract - immunology Gastrointestinal Tract - microbiology Humanities and Social Sciences Immune response Inflammation Inflammation - etiology Inflammation - pathology Inflammatory bowel disease Intestinal microflora Intestine Intestines - immunology Intestines - microbiology Life Sciences Mice Mice, Inbred C57BL Microbiota multidisciplinary Opportunist infection Oral administration Pathogens Science Science (multidisciplinary) Yeasts |
| title | Remodeling of the Candida glabrata cell wall in the gastrointestinal tract affects the gut microbiota and the immune response |
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