Loading…

Fecal microbiota from MRL/lpr mice exacerbates pristane-induced lupus

The roles of gut microbiota in the pathogenesis of SLE have been receiving much attention during recent years. However, it remains unknown how fecal microbiota transplantation (FMT) and microbial metabolites affect immune responses and lupus progression. We transferred fecal microbiota from MRL/lpr...

Full description

Saved in:
Bibliographic Details
Published in:Arthritis research & therapy 2023-03, Vol.25 (1), p.42-42, Article 42
Main Authors: Yi, Xiaoqing, Huang, Cancan, Huang, Chuyi, Zhao, Ming, Lu, Qianjin
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c564t-b882aaf25f95e4540f7b52f94e2ff009fd8353494aef41dd79ec596fcebf3b7d3
cites cdi_FETCH-LOGICAL-c564t-b882aaf25f95e4540f7b52f94e2ff009fd8353494aef41dd79ec596fcebf3b7d3
container_end_page 42
container_issue 1
container_start_page 42
container_title Arthritis research & therapy
container_volume 25
creator Yi, Xiaoqing
Huang, Cancan
Huang, Chuyi
Zhao, Ming
Lu, Qianjin
description The roles of gut microbiota in the pathogenesis of SLE have been receiving much attention during recent years. However, it remains unknown how fecal microbiota transplantation (FMT) and microbial metabolites affect immune responses and lupus progression. We transferred fecal microbiota from MRL/lpr (Lpr) mice and MRL/Mpj (Mpj) mice or PBS to pristane-induced lupus mice and observed disease development. We also screened gut microbiota and metabolite spectrums of pristane-induced lupus mice with FMT via 16S rRNA sequencing, metagenomic sequencing, and metabolomics, followed by correlation analysis. FMT from MRL/lpr mice promoted the pathogenesis of pristane-induced lupus and affected immune cell profiles in the intestine, particularly the plasma cells. The structure and composition of microbial communities in the gut of the FMT-Lpr mice were different from those of the FMT-Mpj mice and FMT-PBS mice. The abundances of specific microbes such as prevotella taxa were predominantly elevated in the gut microbiome of the FMT-Lpr mice, which were positively associated with functional pathways such as cyanoamino acid metabolism. Differential metabolites such as valine and L-isoleucine were identified with varied abundances among the three groups. The abundance alterations of the prevotella taxa may affect the phenotypic changes such as proteinuria levels in the pristane-induced lupus mice. These findings further confirm that gut microbiota play an important role in the pathogenesis of lupus. Thus, altering the gut microbiome may provide a novel way to treat lupus.
doi_str_mv 10.1186/s13075-023-03022-w
format article
fullrecord <record><control><sourceid>gale_doaj_</sourceid><recordid>TN_cdi_doaj_primary_oai_doaj_org_article_56f56f5ae32c4fa18a6f689c7afa6105</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A741673293</galeid><doaj_id>oai_doaj_org_article_56f56f5ae32c4fa18a6f689c7afa6105</doaj_id><sourcerecordid>A741673293</sourcerecordid><originalsourceid>FETCH-LOGICAL-c564t-b882aaf25f95e4540f7b52f94e2ff009fd8353494aef41dd79ec596fcebf3b7d3</originalsourceid><addsrcrecordid>eNptUk1v1DAQjRCIlsIf4IAiceGS1t8fJ1RVLa20CAnB2Zo44yWrbLzYSQv_Hu9uW7oI2ZJH4_eePTOvqt5SckqpUWeZcqJlQxhvCCeMNXfPqmMqtGkUV-z5k_ioepXzihSMZeJldcSVZVpbeVxdXqGHoV73PsW2jxPUIcV1_fnr4mzYpG0ea_wFHlMLE-Z6k_o8wYhNP3azx64e5s2cX1cvAgwZ39yfJ9X3q8tvF9fN4sunm4vzReOlElPTGsMAApPBShRSkKBbyYIVyEIgxIbOcMmFFYBB0K7TFr20KnhsA291x0-qm71uF2Hlyl_WkH67CL3bJWJaOkhT7wd0UoXtBuTMiwDUgArKWK8hgKJEFq2Pe63N3K6x8zhOCYYD0cObsf_hlvHWUUKosVwVhQ_3Cin-nDFPbt1nj8NQ-hPn7Jg2xhCqOC3Q9_9AV3FOY-nVDiWJYkb9RS2hVNCPIZaH_VbUnWtBlebM8oI6_Q-qrA7LuOKIoS_5AwLbE8qMc04YHoukxG2d5PZOcsVJbuckd1dI756255HyYB3-B49Fw1k</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2788506286</pqid></control><display><type>article</type><title>Fecal microbiota from MRL/lpr mice exacerbates pristane-induced lupus</title><source>Publicly Available Content (ProQuest)</source><source>PubMed Central</source><creator>Yi, Xiaoqing ; Huang, Cancan ; Huang, Chuyi ; Zhao, Ming ; Lu, Qianjin</creator><creatorcontrib>Yi, Xiaoqing ; Huang, Cancan ; Huang, Chuyi ; Zhao, Ming ; Lu, Qianjin</creatorcontrib><description>The roles of gut microbiota in the pathogenesis of SLE have been receiving much attention during recent years. However, it remains unknown how fecal microbiota transplantation (FMT) and microbial metabolites affect immune responses and lupus progression. We transferred fecal microbiota from MRL/lpr (Lpr) mice and MRL/Mpj (Mpj) mice or PBS to pristane-induced lupus mice and observed disease development. We also screened gut microbiota and metabolite spectrums of pristane-induced lupus mice with FMT via 16S rRNA sequencing, metagenomic sequencing, and metabolomics, followed by correlation analysis. FMT from MRL/lpr mice promoted the pathogenesis of pristane-induced lupus and affected immune cell profiles in the intestine, particularly the plasma cells. The structure and composition of microbial communities in the gut of the FMT-Lpr mice were different from those of the FMT-Mpj mice and FMT-PBS mice. The abundances of specific microbes such as prevotella taxa were predominantly elevated in the gut microbiome of the FMT-Lpr mice, which were positively associated with functional pathways such as cyanoamino acid metabolism. Differential metabolites such as valine and L-isoleucine were identified with varied abundances among the three groups. The abundance alterations of the prevotella taxa may affect the phenotypic changes such as proteinuria levels in the pristane-induced lupus mice. These findings further confirm that gut microbiota play an important role in the pathogenesis of lupus. Thus, altering the gut microbiome may provide a novel way to treat lupus.</description><identifier>ISSN: 1478-6362</identifier><identifier>ISSN: 1478-6354</identifier><identifier>EISSN: 1478-6362</identifier><identifier>DOI: 10.1186/s13075-023-03022-w</identifier><identifier>PMID: 36927795</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Animals ; Antibodies ; Arthritis ; Autoimmunity ; Complications and side effects ; Development and progression ; Feces ; Flow cytometry ; Genes ; Immunological research ; L-Isoleucine ; Lupus ; Lupus Erythematosus, Systemic - chemically induced ; Lymphatic system ; Medical research ; Metabolomics ; Metagenomic sequencing ; Mice ; Mice, Inbred MRL lpr ; Microbiota ; Pathogenesis ; Prevotella ; RNA, Ribosomal, 16S - genetics ; SLE ; Valine</subject><ispartof>Arthritis research &amp; therapy, 2023-03, Vol.25 (1), p.42-42, Article 42</ispartof><rights>2023. The Author(s).</rights><rights>COPYRIGHT 2023 BioMed Central Ltd.</rights><rights>2023. This work is licensed 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>The Author(s) 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c564t-b882aaf25f95e4540f7b52f94e2ff009fd8353494aef41dd79ec596fcebf3b7d3</citedby><cites>FETCH-LOGICAL-c564t-b882aaf25f95e4540f7b52f94e2ff009fd8353494aef41dd79ec596fcebf3b7d3</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/PMC10018936/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2788506286?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,25731,27901,27902,36989,36990,44566,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36927795$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yi, Xiaoqing</creatorcontrib><creatorcontrib>Huang, Cancan</creatorcontrib><creatorcontrib>Huang, Chuyi</creatorcontrib><creatorcontrib>Zhao, Ming</creatorcontrib><creatorcontrib>Lu, Qianjin</creatorcontrib><title>Fecal microbiota from MRL/lpr mice exacerbates pristane-induced lupus</title><title>Arthritis research &amp; therapy</title><addtitle>Arthritis Res Ther</addtitle><description>The roles of gut microbiota in the pathogenesis of SLE have been receiving much attention during recent years. However, it remains unknown how fecal microbiota transplantation (FMT) and microbial metabolites affect immune responses and lupus progression. We transferred fecal microbiota from MRL/lpr (Lpr) mice and MRL/Mpj (Mpj) mice or PBS to pristane-induced lupus mice and observed disease development. We also screened gut microbiota and metabolite spectrums of pristane-induced lupus mice with FMT via 16S rRNA sequencing, metagenomic sequencing, and metabolomics, followed by correlation analysis. FMT from MRL/lpr mice promoted the pathogenesis of pristane-induced lupus and affected immune cell profiles in the intestine, particularly the plasma cells. The structure and composition of microbial communities in the gut of the FMT-Lpr mice were different from those of the FMT-Mpj mice and FMT-PBS mice. The abundances of specific microbes such as prevotella taxa were predominantly elevated in the gut microbiome of the FMT-Lpr mice, which were positively associated with functional pathways such as cyanoamino acid metabolism. Differential metabolites such as valine and L-isoleucine were identified with varied abundances among the three groups. The abundance alterations of the prevotella taxa may affect the phenotypic changes such as proteinuria levels in the pristane-induced lupus mice. These findings further confirm that gut microbiota play an important role in the pathogenesis of lupus. Thus, altering the gut microbiome may provide a novel way to treat lupus.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Arthritis</subject><subject>Autoimmunity</subject><subject>Complications and side effects</subject><subject>Development and progression</subject><subject>Feces</subject><subject>Flow cytometry</subject><subject>Genes</subject><subject>Immunological research</subject><subject>L-Isoleucine</subject><subject>Lupus</subject><subject>Lupus Erythematosus, Systemic - chemically induced</subject><subject>Lymphatic system</subject><subject>Medical research</subject><subject>Metabolomics</subject><subject>Metagenomic sequencing</subject><subject>Mice</subject><subject>Mice, Inbred MRL lpr</subject><subject>Microbiota</subject><subject>Pathogenesis</subject><subject>Prevotella</subject><subject>RNA, Ribosomal, 16S - genetics</subject><subject>SLE</subject><subject>Valine</subject><issn>1478-6362</issn><issn>1478-6354</issn><issn>1478-6362</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptUk1v1DAQjRCIlsIf4IAiceGS1t8fJ1RVLa20CAnB2Zo44yWrbLzYSQv_Hu9uW7oI2ZJH4_eePTOvqt5SckqpUWeZcqJlQxhvCCeMNXfPqmMqtGkUV-z5k_ioepXzihSMZeJldcSVZVpbeVxdXqGHoV73PsW2jxPUIcV1_fnr4mzYpG0ea_wFHlMLE-Z6k_o8wYhNP3azx64e5s2cX1cvAgwZ39yfJ9X3q8tvF9fN4sunm4vzReOlElPTGsMAApPBShRSkKBbyYIVyEIgxIbOcMmFFYBB0K7TFr20KnhsA291x0-qm71uF2Hlyl_WkH67CL3bJWJaOkhT7wd0UoXtBuTMiwDUgArKWK8hgKJEFq2Pe63N3K6x8zhOCYYD0cObsf_hlvHWUUKosVwVhQ_3Cin-nDFPbt1nj8NQ-hPn7Jg2xhCqOC3Q9_9AV3FOY-nVDiWJYkb9RS2hVNCPIZaH_VbUnWtBlebM8oI6_Q-qrA7LuOKIoS_5AwLbE8qMc04YHoukxG2d5PZOcsVJbuckd1dI756255HyYB3-B49Fw1k</recordid><startdate>20230316</startdate><enddate>20230316</enddate><creator>Yi, Xiaoqing</creator><creator>Huang, Cancan</creator><creator>Huang, Chuyi</creator><creator>Zhao, Ming</creator><creator>Lu, Qianjin</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</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></search><sort><creationdate>20230316</creationdate><title>Fecal microbiota from MRL/lpr mice exacerbates pristane-induced lupus</title><author>Yi, Xiaoqing ; Huang, Cancan ; Huang, Chuyi ; Zhao, Ming ; Lu, Qianjin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c564t-b882aaf25f95e4540f7b52f94e2ff009fd8353494aef41dd79ec596fcebf3b7d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Arthritis</topic><topic>Autoimmunity</topic><topic>Complications and side effects</topic><topic>Development and progression</topic><topic>Feces</topic><topic>Flow cytometry</topic><topic>Genes</topic><topic>Immunological research</topic><topic>L-Isoleucine</topic><topic>Lupus</topic><topic>Lupus Erythematosus, Systemic - chemically induced</topic><topic>Lymphatic system</topic><topic>Medical research</topic><topic>Metabolomics</topic><topic>Metagenomic sequencing</topic><topic>Mice</topic><topic>Mice, Inbred MRL lpr</topic><topic>Microbiota</topic><topic>Pathogenesis</topic><topic>Prevotella</topic><topic>RNA, Ribosomal, 16S - genetics</topic><topic>SLE</topic><topic>Valine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yi, Xiaoqing</creatorcontrib><creatorcontrib>Huang, Cancan</creatorcontrib><creatorcontrib>Huang, Chuyi</creatorcontrib><creatorcontrib>Zhao, Ming</creatorcontrib><creatorcontrib>Lu, Qianjin</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 &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>AUTh Library subscriptions: ProQuest Central</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 Health &amp; Medical Complete (Alumni)</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</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>Arthritis research &amp; therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yi, Xiaoqing</au><au>Huang, Cancan</au><au>Huang, Chuyi</au><au>Zhao, Ming</au><au>Lu, Qianjin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fecal microbiota from MRL/lpr mice exacerbates pristane-induced lupus</atitle><jtitle>Arthritis research &amp; therapy</jtitle><addtitle>Arthritis Res Ther</addtitle><date>2023-03-16</date><risdate>2023</risdate><volume>25</volume><issue>1</issue><spage>42</spage><epage>42</epage><pages>42-42</pages><artnum>42</artnum><issn>1478-6362</issn><issn>1478-6354</issn><eissn>1478-6362</eissn><abstract>The roles of gut microbiota in the pathogenesis of SLE have been receiving much attention during recent years. However, it remains unknown how fecal microbiota transplantation (FMT) and microbial metabolites affect immune responses and lupus progression. We transferred fecal microbiota from MRL/lpr (Lpr) mice and MRL/Mpj (Mpj) mice or PBS to pristane-induced lupus mice and observed disease development. We also screened gut microbiota and metabolite spectrums of pristane-induced lupus mice with FMT via 16S rRNA sequencing, metagenomic sequencing, and metabolomics, followed by correlation analysis. FMT from MRL/lpr mice promoted the pathogenesis of pristane-induced lupus and affected immune cell profiles in the intestine, particularly the plasma cells. The structure and composition of microbial communities in the gut of the FMT-Lpr mice were different from those of the FMT-Mpj mice and FMT-PBS mice. The abundances of specific microbes such as prevotella taxa were predominantly elevated in the gut microbiome of the FMT-Lpr mice, which were positively associated with functional pathways such as cyanoamino acid metabolism. Differential metabolites such as valine and L-isoleucine were identified with varied abundances among the three groups. The abundance alterations of the prevotella taxa may affect the phenotypic changes such as proteinuria levels in the pristane-induced lupus mice. These findings further confirm that gut microbiota play an important role in the pathogenesis of lupus. Thus, altering the gut microbiome may provide a novel way to treat lupus.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>36927795</pmid><doi>10.1186/s13075-023-03022-w</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 1478-6362
ispartof Arthritis research & therapy, 2023-03, Vol.25 (1), p.42-42, Article 42
issn 1478-6362
1478-6354
1478-6362
language eng
recordid cdi_doaj_primary_oai_doaj_org_article_56f56f5ae32c4fa18a6f689c7afa6105
source Publicly Available Content (ProQuest); PubMed Central
subjects Animals
Antibodies
Arthritis
Autoimmunity
Complications and side effects
Development and progression
Feces
Flow cytometry
Genes
Immunological research
L-Isoleucine
Lupus
Lupus Erythematosus, Systemic - chemically induced
Lymphatic system
Medical research
Metabolomics
Metagenomic sequencing
Mice
Mice, Inbred MRL lpr
Microbiota
Pathogenesis
Prevotella
RNA, Ribosomal, 16S - genetics
SLE
Valine
title Fecal microbiota from MRL/lpr mice exacerbates pristane-induced lupus
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-31T04%3A39%3A44IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_doaj_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Fecal%20microbiota%20from%20MRL/lpr%20mice%20exacerbates%20pristane-induced%20lupus&rft.jtitle=Arthritis%20research%20&%20therapy&rft.au=Yi,%20Xiaoqing&rft.date=2023-03-16&rft.volume=25&rft.issue=1&rft.spage=42&rft.epage=42&rft.pages=42-42&rft.artnum=42&rft.issn=1478-6362&rft.eissn=1478-6362&rft_id=info:doi/10.1186/s13075-023-03022-w&rft_dat=%3Cgale_doaj_%3EA741673293%3C/gale_doaj_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c564t-b882aaf25f95e4540f7b52f94e2ff009fd8353494aef41dd79ec596fcebf3b7d3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2788506286&rft_id=info:pmid/36927795&rft_galeid=A741673293&rfr_iscdi=true