Deletion of poly(ADP‑ribose) polymerase-1 changes the composition of the microbiome in the gut
Poly(adenosine diphosphate‑ribose) polymerase (PARP)‑1 is the prototypical PARP enzyme well known for its role in DNA repair and as a pro‑inflammatory protein. Since PARP1 is an important co‑factor of several other pro‑inflammatory proteins, in the present study the possible changes in microbial flo...
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| Veröffentlicht in: | Molecular medicine reports 2018-11, Vol.18 (5), p.4335-4341 |
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| creator | Vida, András Kardos, Gábor Kovács, Tünde Bodrogi, Balázs L Bai, Péter |
| description | Poly(adenosine diphosphate‑ribose) polymerase (PARP)‑1 is the prototypical PARP enzyme well known for its role in DNA repair and as a pro‑inflammatory protein. Since PARP1 is an important co‑factor of several other pro‑inflammatory proteins, in the present study the possible changes in microbial flora of PARP1 knockout mice were investigated. Samples from the duodenum, cecum and feces from wild type and PARP1 knockout C57BL/6J male mice were collected and 16S ribosomal RNA genes were sequenced. Based on the sequencing results, the microbiome and compared samples throughout the lower part of the gastrointestinal system were reconstructed. The present results demonstrated that the lack of PARP1 enzyme only disturbed the microbial flora of the duodenum, where the biodiversity increased in the knockout animals on the species level but decreased on the order level. The most prominent change was the overwhelming abundance of the family Porphyromonadaceae in the duodenum of PARP1‑/‑ animals, which disappeared in the cecum and feces where families were spread out more evenly than in the wild type animals. The findings of the present study may improve current understanding of the role of PARP1 in chronic inflammatory diseases. |
| doi_str_mv | 10.3892/mmr.2018.9474 |
| format | Article |
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Since PARP1 is an important co‑factor of several other pro‑inflammatory proteins, in the present study the possible changes in microbial flora of PARP1 knockout mice were investigated. Samples from the duodenum, cecum and feces from wild type and PARP1 knockout C57BL/6J male mice were collected and 16S ribosomal RNA genes were sequenced. Based on the sequencing results, the microbiome and compared samples throughout the lower part of the gastrointestinal system were reconstructed. The present results demonstrated that the lack of PARP1 enzyme only disturbed the microbial flora of the duodenum, where the biodiversity increased in the knockout animals on the species level but decreased on the order level. The most prominent change was the overwhelming abundance of the family Porphyromonadaceae in the duodenum of PARP1‑/‑ animals, which disappeared in the cecum and feces where families were spread out more evenly than in the wild type animals. The findings of the present study may improve current understanding of the role of PARP1 in chronic inflammatory diseases.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2018.9474</identifier><identifier>PMID: 30221733</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Adenosine ; Adenosine diphosphate ; Animals ; Biodiversity ; Cecum ; Deoxyribonucleic acid ; Diabetes ; Diarrhea ; DNA ; DNA polymerases ; DNA repair ; Duodenum ; Feces ; Gastrointestinal Microbiome ; Genetic aspects ; Genetic Association Studies ; Genotype ; Health aspects ; Host-bacteria relationships ; Host-Pathogen Interactions ; Immune system ; Inflammatory diseases ; Metabolic disorders ; Metabolites ; Mice ; Mice, Knockout ; Microbiomes ; Microbiota (Symbiotic organisms) ; Poly (ADP-Ribose) Polymerase-1 - deficiency ; Poly(ADP-ribose) ; Poly(ADP-ribose) polymerase ; Poly(ADP-ribose) Polymerase 1 ; Proteins ; Ribose ; Ribosomal DNA ; Rodents ; rRNA 16S ; Transcription factors</subject><ispartof>Molecular medicine reports, 2018-11, Vol.18 (5), p.4335-4341</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><rights>Copyright: © Vida et al. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-af63e54c4f82d7c51053acbd522017ff51459ebd8234f37b6d98fc9f8ee6b3fd3</citedby><cites>FETCH-LOGICAL-c482t-af63e54c4f82d7c51053acbd522017ff51459ebd8234f37b6d98fc9f8ee6b3fd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30221733$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vida, András</creatorcontrib><creatorcontrib>Kardos, Gábor</creatorcontrib><creatorcontrib>Kovács, Tünde</creatorcontrib><creatorcontrib>Bodrogi, Balázs L</creatorcontrib><creatorcontrib>Bai, Péter</creatorcontrib><title>Deletion of poly(ADP‑ribose) polymerase-1 changes the composition of the microbiome in the gut</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Poly(adenosine diphosphate‑ribose) polymerase (PARP)‑1 is the prototypical PARP enzyme well known for its role in DNA repair and as a pro‑inflammatory protein. Since PARP1 is an important co‑factor of several other pro‑inflammatory proteins, in the present study the possible changes in microbial flora of PARP1 knockout mice were investigated. Samples from the duodenum, cecum and feces from wild type and PARP1 knockout C57BL/6J male mice were collected and 16S ribosomal RNA genes were sequenced. Based on the sequencing results, the microbiome and compared samples throughout the lower part of the gastrointestinal system were reconstructed. The present results demonstrated that the lack of PARP1 enzyme only disturbed the microbial flora of the duodenum, where the biodiversity increased in the knockout animals on the species level but decreased on the order level. The most prominent change was the overwhelming abundance of the family Porphyromonadaceae in the duodenum of PARP1‑/‑ animals, which disappeared in the cecum and feces where families were spread out more evenly than in the wild type animals. The findings of the present study may improve current understanding of the role of PARP1 in chronic inflammatory diseases.</description><subject>Adenosine</subject><subject>Adenosine diphosphate</subject><subject>Animals</subject><subject>Biodiversity</subject><subject>Cecum</subject><subject>Deoxyribonucleic acid</subject><subject>Diabetes</subject><subject>Diarrhea</subject><subject>DNA</subject><subject>DNA polymerases</subject><subject>DNA repair</subject><subject>Duodenum</subject><subject>Feces</subject><subject>Gastrointestinal Microbiome</subject><subject>Genetic aspects</subject><subject>Genetic Association Studies</subject><subject>Genotype</subject><subject>Health aspects</subject><subject>Host-bacteria relationships</subject><subject>Host-Pathogen Interactions</subject><subject>Immune system</subject><subject>Inflammatory diseases</subject><subject>Metabolic disorders</subject><subject>Metabolites</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Microbiomes</subject><subject>Microbiota (Symbiotic organisms)</subject><subject>Poly (ADP-Ribose) Polymerase-1 - deficiency</subject><subject>Poly(ADP-ribose)</subject><subject>Poly(ADP-ribose) polymerase</subject><subject>Poly(ADP-ribose) Polymerase 1</subject><subject>Proteins</subject><subject>Ribose</subject><subject>Ribosomal DNA</subject><subject>Rodents</subject><subject>rRNA 16S</subject><subject>Transcription factors</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkstu1DAUhiMEoqWwZIsisSmLDL5fNkijtlykSrCAtXGc4xlXSTzYSaXueAVesU-C004LRcgLW7-_8x-do7-qXmK0okqTt8OQVgRhtdJMskfVIZYaNxQh9nj_JlrLg-pZzhcICU64flodUEQIlpQeVt9PoYcpxLGOvt7F_up4ffrl-uevFNqY4c2NNECyGRpcu60dN5DraQu1i8Mu5nBXukhDcCm2IQ5Qh_FG2czT8-qJt32GF_v7qPr2_uzrycfm_POHTyfr88YxRabGekGBM8e8Ip10HCNOrWs7Tspw0nuOGdfQdopQ5qlsRaeVd9orANFS39Gj6t2t725uB-gcjFOyvdmlMNh0ZaIN5uHPGLZmEy-NwJJQjYvB8d4gxR8z5MkMITvoeztCnLMhGCnCGcG6oK__QS_inMYyXqGwkAoLLP5QG9uDCaOPpa9bTM2acy2UYEwWavUfqpwOyj7jCD4U_UFBc1tQlp1zAn8_I0ZmiYQpkTBLJMwSicK_-nsx9_RdBuhv7xqycw</recordid><startdate>20181101</startdate><enddate>20181101</enddate><creator>Vida, András</creator><creator>Kardos, Gábor</creator><creator>Kovács, Tünde</creator><creator>Bodrogi, Balázs L</creator><creator>Bai, Péter</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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Kovács, Tünde ; Bodrogi, Balázs L ; Bai, Péter</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c482t-af63e54c4f82d7c51053acbd522017ff51459ebd8234f37b6d98fc9f8ee6b3fd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adenosine</topic><topic>Adenosine diphosphate</topic><topic>Animals</topic><topic>Biodiversity</topic><topic>Cecum</topic><topic>Deoxyribonucleic acid</topic><topic>Diabetes</topic><topic>Diarrhea</topic><topic>DNA</topic><topic>DNA polymerases</topic><topic>DNA repair</topic><topic>Duodenum</topic><topic>Feces</topic><topic>Gastrointestinal Microbiome</topic><topic>Genetic aspects</topic><topic>Genetic Association Studies</topic><topic>Genotype</topic><topic>Health aspects</topic><topic>Host-bacteria relationships</topic><topic>Host-Pathogen Interactions</topic><topic>Immune system</topic><topic>Inflammatory diseases</topic><topic>Metabolic disorders</topic><topic>Metabolites</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Microbiomes</topic><topic>Microbiota (Symbiotic organisms)</topic><topic>Poly (ADP-Ribose) Polymerase-1 - deficiency</topic><topic>Poly(ADP-ribose)</topic><topic>Poly(ADP-ribose) polymerase</topic><topic>Poly(ADP-ribose) Polymerase 1</topic><topic>Proteins</topic><topic>Ribose</topic><topic>Ribosomal DNA</topic><topic>Rodents</topic><topic>rRNA 16S</topic><topic>Transcription factors</topic><toplevel>online_resources</toplevel><creatorcontrib>Vida, András</creatorcontrib><creatorcontrib>Kardos, Gábor</creatorcontrib><creatorcontrib>Kovács, Tünde</creatorcontrib><creatorcontrib>Bodrogi, Balázs L</creatorcontrib><creatorcontrib>Bai, Péter</creatorcontrib><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>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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 Central UK/Ireland</collection><collection>British Nursing Database</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>Biological Science 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 China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vida, András</au><au>Kardos, Gábor</au><au>Kovács, Tünde</au><au>Bodrogi, Balázs L</au><au>Bai, Péter</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Deletion of poly(ADP‑ribose) polymerase-1 changes the composition of the microbiome in the gut</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2018-11-01</date><risdate>2018</risdate><volume>18</volume><issue>5</issue><spage>4335</spage><epage>4341</epage><pages>4335-4341</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Poly(adenosine diphosphate‑ribose) polymerase (PARP)‑1 is the prototypical PARP enzyme well known for its role in DNA repair and as a pro‑inflammatory protein. Since PARP1 is an important co‑factor of several other pro‑inflammatory proteins, in the present study the possible changes in microbial flora of PARP1 knockout mice were investigated. Samples from the duodenum, cecum and feces from wild type and PARP1 knockout C57BL/6J male mice were collected and 16S ribosomal RNA genes were sequenced. Based on the sequencing results, the microbiome and compared samples throughout the lower part of the gastrointestinal system were reconstructed. The present results demonstrated that the lack of PARP1 enzyme only disturbed the microbial flora of the duodenum, where the biodiversity increased in the knockout animals on the species level but decreased on the order level. The most prominent change was the overwhelming abundance of the family Porphyromonadaceae in the duodenum of PARP1‑/‑ animals, which disappeared in the cecum and feces where families were spread out more evenly than in the wild type animals. The findings of the present study may improve current understanding of the role of PARP1 in chronic inflammatory diseases.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>30221733</pmid><doi>10.3892/mmr.2018.9474</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adenosine Adenosine diphosphate Animals Biodiversity Cecum Deoxyribonucleic acid Diabetes Diarrhea DNA DNA polymerases DNA repair Duodenum Feces Gastrointestinal Microbiome Genetic aspects Genetic Association Studies Genotype Health aspects Host-bacteria relationships Host-Pathogen Interactions Immune system Inflammatory diseases Metabolic disorders Metabolites Mice Mice, Knockout Microbiomes Microbiota (Symbiotic organisms) Poly (ADP-Ribose) Polymerase-1 - deficiency Poly(ADP-ribose) Poly(ADP-ribose) polymerase Poly(ADP-ribose) Polymerase 1 Proteins Ribose Ribosomal DNA Rodents rRNA 16S Transcription factors |
| title | Deletion of poly(ADP‑ribose) polymerase-1 changes the composition of the microbiome in the gut |
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