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Desulfovibrio bacteria enhance alpha-synuclein aggregation in a Caenorhabditis elegans model of Parkinson's disease
The aggregation of the neuronal protein alpha-synuclein (alpha-syn) is a key feature in the pathology of Parkinson's disease (PD). Alpha-syn aggregation has been suggested to be induced in the gut cells by pathogenic gut microbes such as bacteria, which has been shown to be associated with PD....
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Published in: | Frontiers in cellular and infection microbiology 2023-05, Vol.13, p.1181315-1181315 |
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description | The aggregation of the neuronal protein alpha-synuclein (alpha-syn) is a key feature in the pathology of Parkinson's disease (PD). Alpha-syn aggregation has been suggested to be induced in the gut cells by pathogenic gut microbes such as
bacteria, which has been shown to be associated with PD. This study aimed to investigate whether
bacteria induce alpha-syn aggregation.
Fecal samples of ten PD patients and their healthy spouses were collected for molecular detection of
species, followed by bacterial isolation. Isolated
strains were used as diets to feed
nematodes which overexpress human alpha-syn fused with yellow fluorescence protein. Curli-producing
MC4100, which has been shown to facilitate alpha-syn aggregation in animal models, was used as a control bacterial strain, and
LSR11, incapable of producing curli, was used as another control strain. The head sections of the worms were imaged using confocal microscopy. We also performed survival assay to determine the effect of
bacteria on the survival of the nematodes.
Statistical analysis revealed that worms fed
bacteria from PD patients harbored significantly more ( |
doi_str_mv | 10.3389/fcimb.2023.1181315 |
format | article |
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bacteria, which has been shown to be associated with PD. This study aimed to investigate whether
bacteria induce alpha-syn aggregation.
Fecal samples of ten PD patients and their healthy spouses were collected for molecular detection of
species, followed by bacterial isolation. Isolated
strains were used as diets to feed
nematodes which overexpress human alpha-syn fused with yellow fluorescence protein. Curli-producing
MC4100, which has been shown to facilitate alpha-syn aggregation in animal models, was used as a control bacterial strain, and
LSR11, incapable of producing curli, was used as another control strain. The head sections of the worms were imaged using confocal microscopy. We also performed survival assay to determine the effect of
bacteria on the survival of the nematodes.
Statistical analysis revealed that worms fed
bacteria from PD patients harbored significantly more (
<0.001, Kruskal-Wallis and Mann-Whitney U test) and larger alpha-syn aggregates (
<0.001) than worms fed
bacteria from healthy individuals or worms fed
strains. In addition, during similar follow-up time, worms fed
strains from PD patients died in significantly higher quantities than worms fed
LSR11 bacteria (
<0.01). These results suggest that
bacteria contribute to PD development by inducing alpha-syn aggregation.</description><identifier>ISSN: 2235-2988</identifier><identifier>EISSN: 2235-2988</identifier><identifier>DOI: 10.3389/fcimb.2023.1181315</identifier><identifier>PMID: 37197200</identifier><language>eng</language><publisher>Switzerland: Frontiers Media S.A</publisher><subject>alpha-synuclein (alpha-syn) ; alpha-Synuclein - genetics ; alpha-Synuclein - metabolism ; Animals ; C. elegans ; Caenorhabditis elegans - metabolism ; Cellular and Infection Microbiology ; Desulfovibrio ; Escherichia coli - genetics ; Escherichia coli - metabolism ; gut Desulfovibrio bacteria ; Humans ; hydrogen sulfide ; lipopolysaccharides ; Parkinson Disease ; Parkinson’s disease</subject><ispartof>Frontiers in cellular and infection microbiology, 2023-05, Vol.13, p.1181315-1181315</ispartof><rights>Copyright © 2023 Huynh, Takala, Murros, Diwedi and Saris.</rights><rights>Copyright © 2023 Huynh, Takala, Murros, Diwedi and Saris 2023 Huynh, Takala, Murros, Diwedi and Saris</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c469t-ad52b3d7619f6d0d7f4cd355495fe92ef2e909a8842636dc325af1f8ca0b07873</citedby><cites>FETCH-LOGICAL-c469t-ad52b3d7619f6d0d7f4cd355495fe92ef2e909a8842636dc325af1f8ca0b07873</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/PMC10183572/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10183572/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37197200$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huynh, Vy A</creatorcontrib><creatorcontrib>Takala, Timo M</creatorcontrib><creatorcontrib>Murros, Kari E</creatorcontrib><creatorcontrib>Diwedi, Bidhi</creatorcontrib><creatorcontrib>Saris, Per E J</creatorcontrib><title>Desulfovibrio bacteria enhance alpha-synuclein aggregation in a Caenorhabditis elegans model of Parkinson's disease</title><title>Frontiers in cellular and infection microbiology</title><addtitle>Front Cell Infect Microbiol</addtitle><description>The aggregation of the neuronal protein alpha-synuclein (alpha-syn) is a key feature in the pathology of Parkinson's disease (PD). Alpha-syn aggregation has been suggested to be induced in the gut cells by pathogenic gut microbes such as
bacteria, which has been shown to be associated with PD. This study aimed to investigate whether
bacteria induce alpha-syn aggregation.
Fecal samples of ten PD patients and their healthy spouses were collected for molecular detection of
species, followed by bacterial isolation. Isolated
strains were used as diets to feed
nematodes which overexpress human alpha-syn fused with yellow fluorescence protein. Curli-producing
MC4100, which has been shown to facilitate alpha-syn aggregation in animal models, was used as a control bacterial strain, and
LSR11, incapable of producing curli, was used as another control strain. The head sections of the worms were imaged using confocal microscopy. We also performed survival assay to determine the effect of
bacteria on the survival of the nematodes.
Statistical analysis revealed that worms fed
bacteria from PD patients harbored significantly more (
<0.001, Kruskal-Wallis and Mann-Whitney U test) and larger alpha-syn aggregates (
<0.001) than worms fed
bacteria from healthy individuals or worms fed
strains. In addition, during similar follow-up time, worms fed
strains from PD patients died in significantly higher quantities than worms fed
LSR11 bacteria (
<0.01). These results suggest that
bacteria contribute to PD development by inducing alpha-syn aggregation.</description><subject>alpha-synuclein (alpha-syn)</subject><subject>alpha-Synuclein - genetics</subject><subject>alpha-Synuclein - metabolism</subject><subject>Animals</subject><subject>C. elegans</subject><subject>Caenorhabditis elegans - metabolism</subject><subject>Cellular and Infection Microbiology</subject><subject>Desulfovibrio</subject><subject>Escherichia coli - genetics</subject><subject>Escherichia coli - metabolism</subject><subject>gut Desulfovibrio bacteria</subject><subject>Humans</subject><subject>hydrogen sulfide</subject><subject>lipopolysaccharides</subject><subject>Parkinson Disease</subject><subject>Parkinson’s disease</subject><issn>2235-2988</issn><issn>2235-2988</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNpVkctu1DAUQCMEolXpD7BA3sEmgx9xYq8QmvKoVAkWsLZu7OuMS2IPdlKpf0-mM1StN7bv4_hap6reMroRQumP3oap33DKxYYxxQSTL6pzzoWsuVbq5ZPzWXVZyi1dV0e50uJ1dSY6pjtO6XlVrrAso093oc8hkR7sjDkAwbiDaJHAuN9BXe7jYkcMkcAwZBxgDimSw5VsAWPKO-hdmEMhOK7ZWMiUHI4kefIT8p8QS4rvC3GhIBR8U73yMBa8PO0X1e-vX35tv9c3P75dbz_f1LZp9VyDk7wXrmuZ9q2jrvONdULKRkuPmqPnqKkGpRreitZZwSV45pUF2tNOdeKiuj5yXYJbs89hgnxvEgTzEEh5MJDnsH7MCCotWM2E0K5Rve2pZdCBlJyKlkqxsj4dWfuln9BZjHOG8Rn0eSaGnRnSnWGUKSE7vhI-nAg5_V2wzGYKxeI4QsS0FMMVk1xS2sq1lB9LbU6lZPSP7zBqDvbNg31zsG9O9temd08nfGz571r8AzZzre0</recordid><startdate>20230501</startdate><enddate>20230501</enddate><creator>Huynh, Vy A</creator><creator>Takala, Timo M</creator><creator>Murros, Kari E</creator><creator>Diwedi, Bidhi</creator><creator>Saris, Per E J</creator><general>Frontiers Media S.A</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>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20230501</creationdate><title>Desulfovibrio bacteria enhance alpha-synuclein aggregation in a Caenorhabditis elegans model of Parkinson's disease</title><author>Huynh, Vy A ; Takala, Timo M ; Murros, Kari E ; Diwedi, Bidhi ; Saris, Per E J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c469t-ad52b3d7619f6d0d7f4cd355495fe92ef2e909a8842636dc325af1f8ca0b07873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>alpha-synuclein (alpha-syn)</topic><topic>alpha-Synuclein - genetics</topic><topic>alpha-Synuclein - metabolism</topic><topic>Animals</topic><topic>C. elegans</topic><topic>Caenorhabditis elegans - metabolism</topic><topic>Cellular and Infection Microbiology</topic><topic>Desulfovibrio</topic><topic>Escherichia coli - genetics</topic><topic>Escherichia coli - metabolism</topic><topic>gut Desulfovibrio bacteria</topic><topic>Humans</topic><topic>hydrogen sulfide</topic><topic>lipopolysaccharides</topic><topic>Parkinson Disease</topic><topic>Parkinson’s disease</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huynh, Vy A</creatorcontrib><creatorcontrib>Takala, Timo M</creatorcontrib><creatorcontrib>Murros, Kari E</creatorcontrib><creatorcontrib>Diwedi, Bidhi</creatorcontrib><creatorcontrib>Saris, Per E J</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ: Directory of Open Access Journals</collection><jtitle>Frontiers in cellular and infection microbiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huynh, Vy A</au><au>Takala, Timo M</au><au>Murros, Kari E</au><au>Diwedi, Bidhi</au><au>Saris, Per E J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Desulfovibrio bacteria enhance alpha-synuclein aggregation in a Caenorhabditis elegans model of Parkinson's disease</atitle><jtitle>Frontiers in cellular and infection microbiology</jtitle><addtitle>Front Cell Infect Microbiol</addtitle><date>2023-05-01</date><risdate>2023</risdate><volume>13</volume><spage>1181315</spage><epage>1181315</epage><pages>1181315-1181315</pages><issn>2235-2988</issn><eissn>2235-2988</eissn><abstract>The aggregation of the neuronal protein alpha-synuclein (alpha-syn) is a key feature in the pathology of Parkinson's disease (PD). Alpha-syn aggregation has been suggested to be induced in the gut cells by pathogenic gut microbes such as
bacteria, which has been shown to be associated with PD. This study aimed to investigate whether
bacteria induce alpha-syn aggregation.
Fecal samples of ten PD patients and their healthy spouses were collected for molecular detection of
species, followed by bacterial isolation. Isolated
strains were used as diets to feed
nematodes which overexpress human alpha-syn fused with yellow fluorescence protein. Curli-producing
MC4100, which has been shown to facilitate alpha-syn aggregation in animal models, was used as a control bacterial strain, and
LSR11, incapable of producing curli, was used as another control strain. The head sections of the worms were imaged using confocal microscopy. We also performed survival assay to determine the effect of
bacteria on the survival of the nematodes.
Statistical analysis revealed that worms fed
bacteria from PD patients harbored significantly more (
<0.001, Kruskal-Wallis and Mann-Whitney U test) and larger alpha-syn aggregates (
<0.001) than worms fed
bacteria from healthy individuals or worms fed
strains. In addition, during similar follow-up time, worms fed
strains from PD patients died in significantly higher quantities than worms fed
LSR11 bacteria (
<0.01). These results suggest that
bacteria contribute to PD development by inducing alpha-syn aggregation.</abstract><cop>Switzerland</cop><pub>Frontiers Media S.A</pub><pmid>37197200</pmid><doi>10.3389/fcimb.2023.1181315</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | alpha-synuclein (alpha-syn) alpha-Synuclein - genetics alpha-Synuclein - metabolism Animals C. elegans Caenorhabditis elegans - metabolism Cellular and Infection Microbiology Desulfovibrio Escherichia coli - genetics Escherichia coli - metabolism gut Desulfovibrio bacteria Humans hydrogen sulfide lipopolysaccharides Parkinson Disease Parkinson’s disease |
title | Desulfovibrio bacteria enhance alpha-synuclein aggregation in a Caenorhabditis elegans model of Parkinson's disease |
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