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Chlorogenic Acid Ameliorates Post‐Infectious Irritable Bowel Syndrome by Regulating Extracellular Vesicles of Gut Microbes
Post‐infectious irritable bowel syndrome (PI‐IBS) occurs after acute infectious diarrhea, and dysbiosis can be involved in its pathogenesis. Here, the role of chlorogenic acid (CGA) is investigated, a natural compound with several pharmacological properties, in alleviating PI‐IBS in rats. It is eluc...
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Published in: | Advanced science 2023-10, Vol.10 (28), p.e2302798-e2302798 |
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description | Post‐infectious irritable bowel syndrome (PI‐IBS) occurs after acute infectious diarrhea, and dysbiosis can be involved in its pathogenesis. Here, the role of chlorogenic acid (CGA) is investigated, a natural compound with several pharmacological properties, in alleviating PI‐IBS in rats. It is elucidated that the gut microbiota plays a key role in PI‐IBS pathogenesis and that rectal administration of CGA alleviated PI‐IBS by modulating the gut microbiota and its metabolites. CGA supplementation significantly increased fecal
Bacteroides acidifaciens
abundance and glycine levels. Glycine structurally altered
B. acidifacien
s extracellular vesicles (EVs) and enriched functional proteins in the EVs; glycine‐induced EVs alleviated PI‐IBS by reducing inflammation and hypersensitivity of the intestinal viscera and maintaining mucosal barrier function. Moreover,
B. acidifacien
s EVs are enriched in the brain tissue. Thus, CGA mediates the mitigation of PI‐IBS through the gut microbiota and its metabolites. This study proposes a novel mechanism of signal exchange between the gut microenvironment and the host. |
doi_str_mv | 10.1002/advs.202302798 |
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Bacteroides acidifaciens
abundance and glycine levels. Glycine structurally altered
B. acidifacien
s extracellular vesicles (EVs) and enriched functional proteins in the EVs; glycine‐induced EVs alleviated PI‐IBS by reducing inflammation and hypersensitivity of the intestinal viscera and maintaining mucosal barrier function. Moreover,
B. acidifacien
s EVs are enriched in the brain tissue. Thus, CGA mediates the mitigation of PI‐IBS through the gut microbiota and its metabolites. This study proposes a novel mechanism of signal exchange between the gut microenvironment and the host.</description><identifier>ISSN: 2198-3844</identifier><identifier>EISSN: 2198-3844</identifier><identifier>DOI: 10.1002/advs.202302798</identifier><identifier>PMID: 37616338</identifier><language>eng</language><publisher>Weinheim: John Wiley & Sons, Inc</publisher><subject>Bacteria ; bacteroides acidifaciens ; chlorogenic acid ; Colon ; Cytokines ; Extracellular vesicles ; glycine ; Gram-positive bacteria ; Irritable bowel syndrome ; Kinases ; Metabolites ; Microbiota ; Permeability ; PI‐IBS ; Post traumatic stress disorder ; Proteins ; Tumor necrosis factor-TNF</subject><ispartof>Advanced science, 2023-10, Vol.10 (28), p.e2302798-e2302798</ispartof><rights>2023. 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>2023 The Authors. Advanced Science published by Wiley‐VCH GmbH</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3778-f698cf35ea2d38921de06eb9f91da9a521f61e836c081b62eba31f11512292333</citedby><cites>FETCH-LOGICAL-c3778-f698cf35ea2d38921de06eb9f91da9a521f61e836c081b62eba31f11512292333</cites><orcidid>0000-0001-5656-3329</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2873633834/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2873633834?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,25731,27901,27902,36989,36990,44566,53766,53768,74869</link.rule.ids></links><search><creatorcontrib>Zheng, Cihua</creatorcontrib><creatorcontrib>Zhong, Yuchun</creatorcontrib><creatorcontrib>Zhang, Wenming</creatorcontrib><creatorcontrib>Wang, Zhuoya</creatorcontrib><creatorcontrib>Xiao, Haili</creatorcontrib><creatorcontrib>Zhang, Wenjun</creatorcontrib><creatorcontrib>Xie, Jian</creatorcontrib><creatorcontrib>Peng, Xiaogang</creatorcontrib><creatorcontrib>Luo, Jun</creatorcontrib><creatorcontrib>Xu, Wei</creatorcontrib><title>Chlorogenic Acid Ameliorates Post‐Infectious Irritable Bowel Syndrome by Regulating Extracellular Vesicles of Gut Microbes</title><title>Advanced science</title><description>Post‐infectious irritable bowel syndrome (PI‐IBS) occurs after acute infectious diarrhea, and dysbiosis can be involved in its pathogenesis. Here, the role of chlorogenic acid (CGA) is investigated, a natural compound with several pharmacological properties, in alleviating PI‐IBS in rats. It is elucidated that the gut microbiota plays a key role in PI‐IBS pathogenesis and that rectal administration of CGA alleviated PI‐IBS by modulating the gut microbiota and its metabolites. CGA supplementation significantly increased fecal
Bacteroides acidifaciens
abundance and glycine levels. Glycine structurally altered
B. acidifacien
s extracellular vesicles (EVs) and enriched functional proteins in the EVs; glycine‐induced EVs alleviated PI‐IBS by reducing inflammation and hypersensitivity of the intestinal viscera and maintaining mucosal barrier function. Moreover,
B. acidifacien
s EVs are enriched in the brain tissue. Thus, CGA mediates the mitigation of PI‐IBS through the gut microbiota and its metabolites. This study proposes a novel mechanism of signal exchange between the gut microenvironment and the host.</description><subject>Bacteria</subject><subject>bacteroides acidifaciens</subject><subject>chlorogenic acid</subject><subject>Colon</subject><subject>Cytokines</subject><subject>Extracellular vesicles</subject><subject>glycine</subject><subject>Gram-positive bacteria</subject><subject>Irritable bowel syndrome</subject><subject>Kinases</subject><subject>Metabolites</subject><subject>Microbiota</subject><subject>Permeability</subject><subject>PI‐IBS</subject><subject>Post traumatic stress disorder</subject><subject>Proteins</subject><subject>Tumor necrosis factor-TNF</subject><issn>2198-3844</issn><issn>2198-3844</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpdks1u1DAUhSMEolXplrUlNmxm6mvHib1Cw6i0IxWB-NtajnOTeuSJi50URmLBI_CMPAkOU1WUla3ro0_nHp-ieA50CZSyM9PepiWjjFNWK_moOGag5ILLsnz8z_2oOE1pSykFwesS5NPiiNcVVJzL4-LH-tqHGHocnCUr61qy2qF3IZoRE3kf0vj756_N0KEdXZgS2cToRtN4JK_DN_Tk435oY9ghafbkA_aTN6MbenL-fYzGovd5EMkXTM76zAsduZhG8tbZGBpMz4onnfEJT-_Ok-Lzm_NP68vF1buLzXp1tbC8ruWiq5S0HRdoWMulYtAirbBRnYLWKCMYdBWg5JWlEpqKYWM4dAACGFOMc35SbA7cNpitvoluZ-JeB-P030GIvTZxnC1qqZoKDDVgrSwNo4qiaGYXoChg12TWqwPrZmp22Foc8qb-AfThy-CudR9uNVAhZCVZJry8I8TwdcI06p1Lc1ZmwByxZlLUUkApRZa--E-6DVMcclZZVfP5C3mZVcuDKqeaUsTu3g1QPRdFz0XR90XhfwCDJ7Fv</recordid><startdate>20231001</startdate><enddate>20231001</enddate><creator>Zheng, Cihua</creator><creator>Zhong, Yuchun</creator><creator>Zhang, Wenming</creator><creator>Wang, Zhuoya</creator><creator>Xiao, Haili</creator><creator>Zhang, Wenjun</creator><creator>Xie, Jian</creator><creator>Peng, Xiaogang</creator><creator>Luo, Jun</creator><creator>Xu, Wei</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><general>Wiley</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7XB</scope><scope>88I</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>M2O</scope><scope>M2P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-5656-3329</orcidid></search><sort><creationdate>20231001</creationdate><title>Chlorogenic Acid Ameliorates Post‐Infectious Irritable Bowel Syndrome by Regulating Extracellular Vesicles of Gut Microbes</title><author>Zheng, Cihua ; Zhong, Yuchun ; Zhang, Wenming ; Wang, Zhuoya ; Xiao, Haili ; Zhang, Wenjun ; Xie, Jian ; Peng, Xiaogang ; Luo, Jun ; Xu, Wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3778-f698cf35ea2d38921de06eb9f91da9a521f61e836c081b62eba31f11512292333</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Bacteria</topic><topic>bacteroides acidifaciens</topic><topic>chlorogenic acid</topic><topic>Colon</topic><topic>Cytokines</topic><topic>Extracellular vesicles</topic><topic>glycine</topic><topic>Gram-positive bacteria</topic><topic>Irritable bowel syndrome</topic><topic>Kinases</topic><topic>Metabolites</topic><topic>Microbiota</topic><topic>Permeability</topic><topic>PI‐IBS</topic><topic>Post traumatic stress disorder</topic><topic>Proteins</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zheng, Cihua</creatorcontrib><creatorcontrib>Zhong, Yuchun</creatorcontrib><creatorcontrib>Zhang, Wenming</creatorcontrib><creatorcontrib>Wang, Zhuoya</creatorcontrib><creatorcontrib>Xiao, Haili</creatorcontrib><creatorcontrib>Zhang, Wenjun</creatorcontrib><creatorcontrib>Xie, Jian</creatorcontrib><creatorcontrib>Peng, Xiaogang</creatorcontrib><creatorcontrib>Luo, Jun</creatorcontrib><creatorcontrib>Xu, Wei</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>Research Library</collection><collection>Science Journals (ProQuest Database)</collection><collection>Research Library (Corporate)</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 China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Advanced science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zheng, Cihua</au><au>Zhong, Yuchun</au><au>Zhang, Wenming</au><au>Wang, Zhuoya</au><au>Xiao, Haili</au><au>Zhang, Wenjun</au><au>Xie, Jian</au><au>Peng, Xiaogang</au><au>Luo, Jun</au><au>Xu, Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chlorogenic Acid Ameliorates Post‐Infectious Irritable Bowel Syndrome by Regulating Extracellular Vesicles of Gut Microbes</atitle><jtitle>Advanced science</jtitle><date>2023-10-01</date><risdate>2023</risdate><volume>10</volume><issue>28</issue><spage>e2302798</spage><epage>e2302798</epage><pages>e2302798-e2302798</pages><issn>2198-3844</issn><eissn>2198-3844</eissn><abstract>Post‐infectious irritable bowel syndrome (PI‐IBS) occurs after acute infectious diarrhea, and dysbiosis can be involved in its pathogenesis. Here, the role of chlorogenic acid (CGA) is investigated, a natural compound with several pharmacological properties, in alleviating PI‐IBS in rats. It is elucidated that the gut microbiota plays a key role in PI‐IBS pathogenesis and that rectal administration of CGA alleviated PI‐IBS by modulating the gut microbiota and its metabolites. CGA supplementation significantly increased fecal
Bacteroides acidifaciens
abundance and glycine levels. Glycine structurally altered
B. acidifacien
s extracellular vesicles (EVs) and enriched functional proteins in the EVs; glycine‐induced EVs alleviated PI‐IBS by reducing inflammation and hypersensitivity of the intestinal viscera and maintaining mucosal barrier function. Moreover,
B. acidifacien
s EVs are enriched in the brain tissue. Thus, CGA mediates the mitigation of PI‐IBS through the gut microbiota and its metabolites. This study proposes a novel mechanism of signal exchange between the gut microenvironment and the host.</abstract><cop>Weinheim</cop><pub>John Wiley & Sons, Inc</pub><pmid>37616338</pmid><doi>10.1002/advs.202302798</doi><orcidid>https://orcid.org/0000-0001-5656-3329</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Bacteria bacteroides acidifaciens chlorogenic acid Colon Cytokines Extracellular vesicles glycine Gram-positive bacteria Irritable bowel syndrome Kinases Metabolites Microbiota Permeability PI‐IBS Post traumatic stress disorder Proteins Tumor necrosis factor-TNF |
title | Chlorogenic Acid Ameliorates Post‐Infectious Irritable Bowel Syndrome by Regulating Extracellular Vesicles of Gut Microbes |
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